896 results match your criteria Biochimica Et Biophysica Acta-molecular Basis Of Disease[Journal]


Animal models for hepatocellular carcinoma.

Biochim Biophys Acta Mol Basis Dis 2019 May 10;1865(5):993-1002. Epub 2018 Aug 10.

Centenary Institute, The University of Sydney, Newtown, New South Wales, 2042, Australia; The University of Sydney Faculty of Medicine and Health, New South Wales, 2006, Australia. Electronic address:

Hepatocellular carcinoma (HCC) represents ~90% of all cases of primary liver cancer and occurs predominantly in patients with underlying chronic liver disease and cirrhosis. Establishing appropriate animal models for HCC is required for basic and translational studies, especially the models that can recapitulate one of the human disease settings. Current animal models can be categorized as chemically-induced, genetically-engineered, xenograft, or a combination of these with each other or with a metabolic insult. Read More

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http://dx.doi.org/10.1016/j.bbadis.2018.08.009DOI Listing

Outside the liver box: The gut microbiota as pivotal modulator of liver diseases.

Biochim Biophys Acta Mol Basis Dis 2019 May 6;1865(5):912-919. Epub 2018 Jul 6.

Sahlgrenska Academy, Institute of Medicine, Department of Molecular and Clinical Medicine, Wallenberg Laboratory, University of Gothenburg, S-413 45 Gothenburg, Sweden. Electronic address:

The gut microbiota affects host physiology and has evolved as an important contributor to health and disease. Gut and liver are closely connected and communicate via the portal vein and the biliary system so the liver is constantly exposed to gut-derived bacterial products and metabolites. The intestinal barrier is important for maintaining physical and functional separation between microbes in the gut and the interior of the host and disruption of the barrier function can lead to bacterial translocation and increased leakage of bacterial metabolites. Read More

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http://dx.doi.org/10.1016/j.bbadis.2018.07.004DOI Listing

Animal models of drug-induced liver injury.

Biochim Biophys Acta Mol Basis Dis 2019 May 3;1865(5):1031-1039. Epub 2018 Sep 3.

Dept. of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA. Electronic address:

Drug-induced liver injury (DILI) presents unique challenges for consumers, clinicians, and regulators. It is the most common cause of acute liver failure in the US. It is also one of the most common reasons for termination of new drugs during pre-clinical testing and withdrawal of new drugs post-marketing. Read More

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http://dx.doi.org/10.1016/j.bbadis.2018.08.037DOI Listing

MICAL2 is expressed in cancer associated neo-angiogenic capillary endothelia and it is required for endothelial cell viability, motility and VEGF response.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 17. Epub 2019 Apr 17.

Scuola Superiore Sant'Anna, Institute of Life Sciences, 56124 Pisa, Italy. Electronic address:

The capacity of inducing angiogenesis is a recognized hallmark of cancer cells. The cancer microenvironment, characterized by hypoxia and inflammatory signals, promotes proliferation, migration and activation of quiescent endothelial cells (EC) from surrounding vascular network. Current anti-angiogenic drugs present side effects, temporary efficacy, and issues of primary resistance, thereby calling for the identification of new therapeutic targets. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09254439193011
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http://dx.doi.org/10.1016/j.bbadis.2019.04.008DOI Listing
April 2019
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Metformin ameliorates endotoxemia-induced endothelial pro-inflammatory responses via AMPK-dependent mediation of HDAC5 and KLF2.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 16. Epub 2019 Apr 16.

Department of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, PR China. Electronic address:

Exaggerated endothelial pro-inflammatory response is a hallmark in the early stage of sepsis and contributes to the subsequent tissue injury and organ failure. The anti-inflammatory effects of AMP-activated protein kinase (AMPK) activator metformin in sepsis has been revealed. However, the underlying mechanisms remain not fully understood. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09254439193012
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http://dx.doi.org/10.1016/j.bbadis.2019.04.009DOI Listing
April 2019
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The metastasis suppressor, NDRG1, differentially modulates the ER stress response in the presence and absence of the anti-cancer agent, Dp44mT.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 11. Epub 2019 Apr 11.

Molecular Pharmacology and Pathology Program, Discipline of Pathology and Bosch Institute, Medical Foundation Building (K25), The University of Sydney, Sydney, New South Wales 2006, Australia; Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya 466-8550, Japan. Electronic address:

The metastasis suppressor, N-myc downstream regulated gene-1 (NDRG1), is a stress response protein that is involved in the inhibition of multiple oncogenic signaling pathways. Initial studies have linked NDRG1 and the endoplasmic reticulum (ER) stress response. Considering this, we extensively examined the mechanism by which NDRG1 regulates the ER stress response in pancreatic and colon cancer cells. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.007DOI Listing

Dietary cholesterol is essential to mast cell activation and associated obesity and diabetes in mice.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 9. Epub 2019 Apr 9.

Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address:

Mast cell (MC) deficiency in Kit mice and inhibition with disodium chromoglycate (DSCG) or ketotifen reduced obesity and diabetes in mice on a high-cholesterol (1.25%) Western diet. Yet, Kit-independent MC-deficient mice and mice treated with DSCG disproved MC function in obesity and diabetes when mice are fed a high-fat diet (HFD) that contains no cholesterol. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.006DOI Listing
April 2019
2 Reads
4.882 Impact Factor

Role of proteases in dysfunctional placental vascular remodelling in preeclampsia.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 5. Epub 2019 Apr 5.

Department of Physiology, Faculty of Pharmacy, Universidad de Sevilla, Seville E-41012, Spain; University of Queensland Centre for Clinical Research (UQCCR), Faculty of Medicine and Biomedical Sciences, University of Queensland, Herston, 4029, Queensland, Australia; Cellular and Molecular Physiology Laboratory (CMPL), Department of Obstetrics, Division of Obstetrics and Gynaecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile. Electronic address:

Preeclampsia is a syndrome characterised by vascular dysfunction, impaired angiogenesis, and hypertension during pregnancy. Even when the precise pathophysiology of preeclampsia remains elusive, impaired vascular remodelling and placental angiogenesis in the placental villi and defective trophoblast invasion of the uterus are proposed as crucial mechanisms in this syndrome. Reduced trophoblast invasion leads to reduced uteroplacental blood flow and oxygen availability and increased oxidative stress. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.004DOI Listing
April 2019
3 Reads

Novel cell line models to study mechanisms and overcoming strategies of proteasome inhibitor resistance in multiple myeloma.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 4. Epub 2019 Apr 4.

University Hospital of Würzburg, Comprehensive Cancer Center Mainfranken, Translational Oncology, Würzburg, Germany.

Experimental data on resistance mechanisms of multiple myeloma (MM) to ixazomib (IXA), a second-generation proteasome inhibitor (PI), are currently lacking. We generated MM cell lines with a 10-fold higher resistance to IXA as their sensitive counterparts, and observed cross-resistance towards the PIs carfilzomib (CFZ) and bortezomib (BTZ). Analyses of the IXA-binding proteasome subunits PSMB5 and PSMB1 show increased PSMB5 expression and activity in all IXA-resistant MM cells, and upregulated PSMB1 expression in IXA-resistant AMO1 cells. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.003DOI Listing
April 2019
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Reduction of SIRT1 blunts the protective effects of ischemic post-conditioning in diabetic mice by impairing the Akt signaling pathway.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 4. Epub 2019 Apr 4.

Department of Cardiology, Xijing Hospital, Fourth Military Medical University, China. Electronic address:

Ischemic post-conditioning (IPO) activates Akt signaling to confer cardioprotection. The responsiveness of diabetic hearts to IPO is impaired. We hypothesized that decreased cardiac SIRT1, a positive regulator of Akt, may be responsible for the impaired responsiveness of diabetic hearts to IPO-mediated cardioprotection. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.005DOI Listing
April 2019
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Epigenetic silencing of genes enhanced by collective role of reactive oxygen species and MAPK signaling downstream ERK/Snail axis: Ectopic application of hydrogen peroxide repress CDH1 gene by enhanced DNA methyltransferase activity in human breast cancer.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 4. Epub 2019 Apr 4.

Epigenetics and Cancer Research Laboratory, Biochemistry and Molecular Biology Group, Department of Life Science, National Institute of Technology, Rourkela, Odisha 769008, India. Electronic address:

Loss of E-cadherin and epithelial to mesenchymal transition (EMT) are key steps in cancer progression. Reactive oxygen species (ROS) play significant roles in cellular physiology and homeostasis. Roles of E-cadherin, EMT and ROS are intriguingly illustrated in many cancers without focusing their collective concert during cancer progression. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.002DOI Listing
April 2019
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4.882 Impact Factor

TRPC channels: Regulation, dysregulation and contributions to chronic kidney disease.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 4. Epub 2019 Apr 4.

Department of Biology and Biochemistry, University of Houston, Houston, TX, USA.

Mutations in the gene encoding canonical transient receptor potential-6 (TRPC6) channels result in severe nephrotic syndromes that typically lead to end-stage renal disease. Many but not all of these mutations result in a gain in the function of the resulting channel protein. Since those observations were first made, substantial work has supported the hypothesis that TRPC6 channels can also contribute to progression of acquired (non-genetic) glomerular diseases, including primary and secondary FSGS, glomerulosclerosis during autoimmune glomerulonephritis, and possibly in type-1 diabetes. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.04.001DOI Listing
April 2019
2 Reads

DNA repair fidelity in stem cell maintenance, health, and disease.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 4. Epub 2019 Apr 4.

Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Centre, Lubbock, TX 79430, United States of America. Electronic address:

Stem cells are a sub population of cell types that form the foundation of our body, and have the potential to replicate, replenish and repair limitlessly to maintain the tissue and organ homeostasis. Increased lifetime and frequent replication set them vulnerable for both exogenous and endogenous agents-induced DNA damage compared to normal cells. To counter these damages and preserve genetic information, stem cells have evolved with various DNA damage response and repair mechanisms. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.017DOI Listing
April 2019
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Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 2. Epub 2019 Apr 2.

CNR, Institute of Biomedicine and Molecular Immunology, Palermo, Italy.

Background: Allergic rhinitis is characterized by a remodeling of nasal epithelium. Since the Notch and TGF-β signaling pathways are known to be involved in cell differentiation and remodeling processes and leptin adipokine has already been identified as a marker for homeostasis in human bronchial and nasal epithelial cells of asthmatics, roles played by these pathways have been investigated for chronic allergic rhinitis.

Methods: The leptin/leptin receptor expression has been investigated in a study with 40 biopsies from allergic (AR, n = 18) and non-allergic (C, n = 22) inferior turbinates, using immunohistochemistry, immunofluorescence staining and RT-PCR. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.016DOI Listing
April 2019
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Mitochondrial ALDH2 protects against lipopolysaccharide-induced myocardial contractile dysfunction by suppression of ER stress and autophagy.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 1. Epub 2019 Apr 1.

Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA; Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Fudan University Zhongshan Hospital, Shanghai 200032, China. Electronic address:

Lipopolysaccharide (LPS), an essential component of outer membrane of the Gram-negative bacteria, plays a pivotal role in myocardial anomalies in sepsis. Recent evidence depicted an essential role for mitochondrial aldehyde dehydrogenase (ALDH2) in cardiac homeostasis. This study examined the effect of ALDH2 on endotoxemia-induced cardiac anomalies. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.015DOI Listing

Mitochondrial fusion and maintenance of mitochondrial homeostasis in diabetic retinopathy.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 25. Epub 2019 Mar 25.

Kresge Eye Institute, Department of Ophthalmology, Visual & Anatomical Sciences, Wayne State University, Detroit, MI, United States of America. Electronic address:

Mitochondria are dynamic in structure, and undergo continuous fusion-fission to maintain their homeostasis. In diabetes, retinal mitochondria are swollen, their membrane is damaged and mitochondrial fusion protein, mitofusin 2 (Mfn2), is decreased. DNA methylation machinery is also activated and methylation status of genes implicated in mitochondrial damage and biogenesis is altered. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.013DOI Listing
March 2019
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4.882 Impact Factor

LRP1 promotes synthetic phenotype of pulmonary artery smooth muscle cells in pulmonary hypertension.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 22. Epub 2019 Mar 22.

Department of Biochemistry, Universities of Giessen and Marburg Lung Center, Giessen, Germany. Electronic address:

Pulmonary hypertension (PH) is characterized by a thickening of the distal pulmonary arteries caused by medial hypertrophy, intimal proliferation and vascular fibrosis. Low density lipoprotein receptor-related protein 1 (LRP1) maintains vascular homeostasis by mediating endocytosis of numerous ligands and by initiating and regulating signaling pathways. Here, we demonstrate the increased levels of LRP1 protein in the lungs of idiopathic pulmonary arterial hypertension (IPAH) patients, hypoxia-exposed mice, and monocrotaline-treated rats. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.012DOI Listing
March 2019
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Cartilage biomechanics: A key factor for osteoarthritis regenerative medicine.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 22. Epub 2019 Mar 22.

Biopathology and Regenerative Medicine Institute (IBIMER), Centre for Biomedical Research, University of Granada, Granada E-18100, Spain; Excellence Research Unit "Modeling Nature" (MNat), University of Granada, Spain; Biosanitary Research Institute of Granada (ibs.GRANADA), University Hospitals of Granada-University of Granada, Granada E-18071, Spain; Department of Human Anatomy and Embryology, Faculty of Medicine, University of Granada, Granada E-18016, Spain. Electronic address:

Osteoarthritis (OA) is a joint disorder that is highly extended in the global population. Several researches and therapeutic strategies have been probed on OA but without satisfactory long-term results in joint replacement. Recent evidences show how the cartilage biomechanics plays a crucial role in tissue development. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.011DOI Listing
March 2019
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Chemokine (C-C motif) ligand 2 gene ablation protects low-density lipoprotein and paraoxonase-1 double deficient mice from liver injury, oxidative stress and inflammation.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 21. Epub 2019 Mar 21.

Universitat Rovira i Virgili, Department of Medicine and Surgery, Reus, Spain; Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain; The Campus of International Excellence Southern Catalonia, Tarragona, Spain. Electronic address:

The risk of non-alcoholic fatty liver disease increases with obesity. Vulnerability to oxidative stress and/or inflammation represents a crucial step in non-alcoholic fatty liver disease progression through abnormal metabolic responses. In this study, we investigated the role of CCL2 gene ablation in mice that were double deficient in low density lipoprotein receptor and in paraoxonase-1. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.006DOI Listing
March 2019
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Intestinal vitamin D receptor modulates lipid metabolism, adipose tissue inflammation and liver steatosis in obese mice.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 21. Epub 2019 Mar 21.

University Hospital Würzburg, Division of Hepatology, Würzburg, Germany; University Hospital Zürich, Division of Gastroenterology and Hepatology, Zürich, Switzerland. Electronic address:

Objective: Hypovitaminosis D is common in the obese population and patients suffering from obesity-associated disorders such as type 2 diabetes and fatty liver disease, resulting in suggestions for vitamin D supplementation as a potential therapeutic option. However, the pathomechanistic contribution of the vitamin D-vitamin D receptor (VDR) axis to metabolic disorders is largely unknown.

Methods: We analyzed the pathophysiological role of global and intestinal VDR signaling in diet-induced obesity (DIO) using global Vdr-/- mice and mice re-expressing an intestine-specific human VDR transgene in the Vdr deficient background (Vdr-/- hTg). Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.007DOI Listing
March 2019
2 Reads

Lysosome motility and distribution: Relevance in health and disease.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 21. Epub 2019 Mar 21.

Department of Gastroenterology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile. Electronic address:

Lysosomes are dynamic organelles, which can fuse with a variety of targets and undergo constant regeneration. They can move along microtubules in a retrograde and anterograde fashion by using motor proteins, kinesin and dynein, being main players in extracellular secretion, intracellular components degradation and recycling. Moreover, lysosomes interact with other intracellular organelles to regulate their turnover, such as ER, mitochondria and peroxisomes. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.009DOI Listing

Role of OCT4 in cancer stem-like cells and chemotherapy resistance.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 21. Epub 2019 Mar 21.

Cancer Center, Department of Pediatrics, Pharmacology & Neuroscience, School of Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Electronic address:

Cancer stem-like cells (CSCs) contribute to the tumorigenicity, progression, and chemoresistance of cancers. It is not known whether CSCs arise from normal stem cells or if they arise from differentiated cancer cells by acquiring self-renewal features. These CSCs share stem cell markers that normal stem cells express. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.005DOI Listing
March 2019
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PID1 regulates insulin-dependent glucose uptake by controlling intracellular sorting of GLUT4-storage vesicles.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 21. Epub 2019 Mar 21.

Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg Eppendorf, 20246 Hamburg, Germany. Electronic address:

The phosphotyrosine interacting domain-containing protein 1 (PID1) serves as a cytosolic adaptor protein of the LDL receptor-related protein 1 (LRP1). By regulating its intracellular trafficking, PID1 controls the hepatic, LRP1-dependent clearance of pro-atherogenic lipoproteins. In adipose and muscle tissues, LRP1 is present in endosomal storage vesicles containing the insulin-responsive glucose transporter 4 (GLUT4). Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.010DOI Listing

Dystrobrevin is required postsynaptically for homeostatic potentiation at the Drosophila NMJ.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 21. Epub 2019 Mar 21.

Department of Pharmacology, Faculty of Medicine, Chiang Mai University, Thailand; Research Center of Pharmaceutical Nanotechnology, Chiang Mai University, Thailand; Laboratory of Developmental Neurobiology, Department of Molecular Cell Biology, Leiden University Medical Center, the Netherlands. Electronic address:

Evolutionarily conserved homeostatic systems have been shown to modulate synaptic efficiency at the neuromuscular junctions of organisms. While advances have been made in identifying molecules that function presynaptically during homeostasis, limited information is currently available on how postsynaptic alterations affect presynaptic function. We previously identified a role for postsynaptic Dystrophin in the maintenance of evoked neurotransmitter release. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.008DOI Listing
March 2019
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Using induced pluripotent stem cell neuronal models to study neurodegenerative diseases.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 18. Epub 2019 Mar 18.

Department of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Center for Mitochondrial Diseases, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. Electronic address:

Current application of human induced pluripotent stem cells (hiPSCs) technology in patient-specific models of neurodegenerative disorders recapitulate some of key phenotypes of diseases, representing disease-specific cellular modeling and providing a unique platform for therapeutics development. We review recent efforts toward advancing hiPSCs-derived neuronal cell types and highlight their potential use for the development of more complex in vitro models of neurodegenerative diseases by focusing on Alzheimer's disease, Parkinson's disease, Huntington's disease and Amyotrophic lateral sclerosis. We present evidence from previous works on the important phenotypic changes of various neuronal types in these neurological diseases. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.004DOI Listing
March 2019
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Corrigendum to "MLL3 enhances the transcription of PD-L1 and regulates anti-tumor immunity" [Biochim. Biophys. Acta, Mol. Basis Dis. 1865 (2) (Feb 1, 2019) 454-463].

Biochim Biophys Acta Mol Basis Dis 2019 Mar 18. Epub 2019 Mar 18.

Department of Urology, The Second Xiangya Hospital, Central South University, Changsha 410011, China. Electronic address:

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http://dx.doi.org/10.1016/j.bbadis.2019.01.030DOI Listing
March 2019
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Pinealectomy or light exposure exacerbates biliary damage and liver fibrosis in cholestatic rats through decreased melatonin synthesis.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 16. Epub 2019 Mar 16.

Department of Medical Physiology, Texas A&M University, College of Medicine, United States of America. Electronic address:

Melatonin, a neuroendocrine hormone synthesized by the pineal gland and cholangiocytes, decreases biliary hyperplasia and liver fibrosis during cholestasis-induced biliary injury via melatonin-dependent autocrine signaling through increased biliary arylalkylamine N-acetyltransferase (AANAT) expression and melatonin secretion, downregulation of miR-200b and specific circadian clock genes. Melatonin synthesis is decreased by pinealectomy (PINX) or chronic exposure to light. We evaluated the effect of PINX or prolonged light exposure on melatonin-dependent modulation of biliary damage/ductular reaction/liver fibrosis. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.002DOI Listing
March 2019
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GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 16. Epub 2019 Mar 16.

Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City, Mexico; Laboratorio de Medicina Experimental, Unidad de Medicina Translacional, Instituto de Investigaciones Biomédicas, UNAM/Instituto Nacional de Cardiología Ignacio Chavez, Mexico City, Mexico. Electronic address:

Growth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features, despite some controversies in age-related studies. GDF11 has been poorly investigated in cancer, particularly in those with stemness capacity, such as hepatocellular carcinoma (HCC), one of the most aggressive cancers worldwide. Here, we focused on investigating the effects of GDF11 in liver cancer cells. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09254439193007
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http://dx.doi.org/10.1016/j.bbadis.2019.03.003DOI Listing
March 2019
4 Reads

Interactions between cadherin-11 and platelet-derived growth factor receptor-alpha signaling link cell adhesion and proliferation.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 13. Epub 2019 Mar 13.

Division of Rheumatology, Department of Medicine, University of Washington, 750 Republican St, Seattle, WA 98019, USA; Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, 75 Francis St, Boston, MA 02115, USA. Electronic address:

Cadherins are homophilic cell-to-cell adhesion molecules that help cells respond to environmental changes. Newly formed cadherin junctions are associated with increased cell phosphorylation, but the pathways driving this signaling response are largely unknown. Since cadherins have no intrinsic signaling activity, this phosphorylation must occur through interactions with other signaling molecules. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.03.001DOI Listing
March 2019
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Mutation in NADPH oxidase 3 (NOX3) impairs SHH signaling and increases cerebellar neural stem/progenitor cell proliferation.

Biochim Biophys Acta Mol Basis Dis 2019 Mar 8. Epub 2019 Mar 8.

Department of Biochemistry, Laboratory of Neurobiology, Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), Brazil. Electronic address:

Abnormalities in cerebellar structure and function may cause ataxia, a neurological dysfunction of motor coordination. In the course of the present study, we characterized a mutant mouse lineage with an ataxia-like phenotype. We localized the mutation on chromosome 17 and mapped it to position 1534 of the Nox3 gene, resulting in p. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.022DOI Listing

The role of mitochondrial cardiolipin in heart function and its implication in cardiac disease.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 26;1865(4):810-821. Epub 2018 Aug 26.

Institute of Cellular Biochemistry, University Medical Center Göttingen, D-37073 Göttingen, Germany; Max Planck Institute for Biophysical Chemistry, D-37077 Göttingen, Germany. Electronic address:

Mitochondria play an essential role in the energy metabolism of the heart. Many of the essential functions are associated with mitochondrial membranes and oxidative phosphorylation driven by the respiratory chain. Mitochondrial membranes are unique in the cell as they contain the phospholipid cardiolipin. Read More

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http://dx.doi.org/10.1016/j.bbadis.2018.08.025DOI Listing
April 2019
3 Reads

Impact of exercise training on cardiovascular disease and risk.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 28;1865(4):728-734. Epub 2018 Aug 28.

Department of Molecular and Experimental Cardiology, TU Dresden, Heart Center Dresden, Dresden, Germany.

Epidemiological studies in large cohorts support the notion that physical fitness is associated with reduced cardiovascular mortality and hospitalization due to cardiovascular disease. During the last 20 years even the concept of resting inactive after a myocardial infarction has dramatically changed and nowadays patients are mobilized and included into exercise training programs very shortly after the insult. Unfortunately, these beneficial effects of exercise training are independent of the genetic background and are only observed in case the training program is not paused for a longer time. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S09254439183030
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http://dx.doi.org/10.1016/j.bbadis.2018.08.019DOI Listing
April 2019
6 Reads

Reduced biliverdin reductase-A levels are associated with early alterations of insulin signaling in obesity.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 28. Epub 2019 Feb 28.

Department of Biochemical Sciences "A. Rossi-Fanelli" Sapienza University of Rome, Rome, Italy. Electronic address:

Biliverdin reductase-A (BVR-A) is a serine/threonine/tyrosine kinase involved in the regulation of insulin signaling. In vitro studies have demonstrated that BVR-A is a substrate of the insulin receptor and regulates IRS1 by avoiding its aberrant activation, and in animal model of obesity the loss of hepatic BVR-A has been associated with glucose/insulin alterations and fatty liver disease. However, no studies exist in humans. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.021DOI Listing
February 2019
4 Reads

Inflammation-dependent ISG15 upregulation mediates MIA-induced dendrite damages and depression by disrupting NEDD4/Rap2A signaling.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 28. Epub 2019 Feb 28.

Department of Pathophysiology, Key Laboratory of Ministry of Education of China for Neurological Disorders, School of Basic Medicine of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China. Electronic address:

Background: Maternal immune activation (MIA) is an independent risk factor for psychiatric disorders including depression spectrum in the offsprings, but the molecular mechanism is unclear. Recent studies show that interferon-stimulated gene-15 (ISG15) is involved in inflammation and neuronal dendrite development; here we studied the role of ISG15 in MIA-induced depression and the underlying mechanisms.

Methods: By vena caudalis injecting polyinosinic: polycytidylic acid (poly I:C) into the pregnant rats to mimic MIA, we used AAV or lentivirus to introduce or silence ISG15 expression. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.020DOI Listing
February 2019
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Preface - Animal models in liver disease.

Biochim Biophys Acta Mol Basis Dis 2019 May 28;1865(5):867-868. Epub 2019 Feb 28.

Department of Gastroenterology and Hepatology, Medical University Graz, Austria.

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http://dx.doi.org/10.1016/j.bbadis.2019.02.004DOI Listing

Cancer cells stemness: A doorstep to targeted therapy.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 26. Epub 2019 Feb 26.

Department of Immunotherapeutics and Biotechnology, and Center for Tumor Immunology and Targeted Cancer Therapy, Texas Tech University Health Sciences Center, Abilene, TX 79601, USA. Electronic address:

Recent advances in research on cancer have led to understand the pathogenesis of cancer and development of new anticancer drugs. Despite of these advancements, many tumors have been found to recur, undergo metastasis and develop resistance to therapy. Accumulated evidences suggest that small population of cancer cells known as cancer stem cells (CSC) are responsible for reconstitution and propagation of the disease. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.019DOI Listing
February 2019
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NLRX1 regulates TNF-α-induced mitochondria-lysosomal crosstalk to maintain the invasive and metastatic potential of breast cancer cells.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 23. Epub 2019 Feb 23.

Department of Biochemistry, Faculty of Science, The M.S. University of Baroda, Vadodara 390002, Gujarat, India. Electronic address:

An increased level of proinflammatory cytokines, including TNF-α in tumor microenvironment regulates the bioenergetic capacity, immune evasion and survival of cancer cells. Emerging evidences suggest that mitochondrial immune signaling proteins modulates mitochondrial bioenergetic capacity, in addition to the regulation of innate immune response. The optimal oxidative phosphorylation (OxPhos) capacity is required for the maintenance of functional lysosomes and autophagy flux. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.018DOI Listing
February 2019
6 Reads
4.882 Impact Factor

Mutant huntingtin inhibits the mitochondrial unfolded protein response by impairing ABCB10 mRNA stability.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 23. Epub 2019 Feb 23.

Department of Neurobiology, Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing 211166, Jiangsu, China. Electronic address:

Numerous studies have shown that mitochondrial dysfunction contributes to consequential phenotypes of Huntington's disease (HD), a fatal and inherited neurodegenerative disease caused by the expanded CAG repeats in the N-terminus of the huntingtin (Htt) gene. To maintain proper function, mitochondria develop a dedicated protein quality control mechanism by activating a stress response termed the mitochondrial unfolded protein response (UPR). Defects in the UPR have been linked to aging and are also associated with neurodegenerative diseases. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.015DOI Listing
February 2019
1 Read
4.882 Impact Factor

Genetics and Epigenetics in Aging and Longevity: Myths and Truths.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 21. Epub 2019 Feb 21.

Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, 210032, PR China; Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071, USA. Electronic address:

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http://dx.doi.org/10.1016/j.bbadis.2019.02.005DOI Listing
February 2019

Deficiency of heat shock protein A12A promotes browning of white adipose tissues in mice.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 22. Epub 2019 Feb 22.

Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China. Electronic address:

Browning of white adipose tissues (WAT) is critical for a variety of physiological and pathophysiological events. Given the limited understanding in molecular control of WAT browning, further research is needed. Heat shock protein A12A (HSPA12A) is a new member of multigene Hsp70 family. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.017DOI Listing
February 2019
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Mitochondrial and calcium perturbations in rat CNS neurons induce calpain-cleavage of Parkin: Phosphatase inhibition stabilizes pSerParkin reducing its calpain-cleavage.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 21. Epub 2019 Feb 21.

Department of Biological Sciences, Hunter College and Graduate Center, City University of New York, NY 10065, USA. Electronic address:

Mitochondrial impairment and calcium (Ca) dyshomeostasis are associated with Parkinson's disease (PD). When intracellular ATP levels are lowered, Ca-ATPase pumps are impaired causing cytoplasmic Ca to be elevated and calpain activation. Little is known about the effect of calpain activation on Parkin integrity. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.016DOI Listing
February 2019
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Endothelial dysfunction in pregnancy metabolic disorders.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 19. Epub 2019 Feb 19.

Departamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, 8370146 Santiago, Chile; Millennium Institute on Immunology and Immunotherapy, 8331150 Santiago, Chile. Electronic address:

In recent years, the vascular endothelium has gained attention as a key player in the initiation and development of pregnancy disorders. Endothelium acts as an endocrine organ that preserves the homeostatic balance by responding to changes in metabolic status. However, in metabolic disorders, endothelial cells adopt a dysfunctional function, losing their normal responsiveness. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.009DOI Listing
February 2019
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Long non-coding RNA cytoskeleton regulator RNA (CYTOR) modulates pathological cardiac hypertrophy through miR-155-mediated IKKi signaling.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 19. Epub 2019 Feb 19.

Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan 430060, China; Department of Cardiology, The Fifth Affiliated Hospital of Xin Jiang Medical University, Urumchi 830001, China; Qianjiang Central Hospital of Hubei Province, Qianjiang 433100, China. Electronic address:

Pathological cardiac hypertrophy, which may lead to heart failure and sudden death, can be affected by multiple factors. In our previous study, we revealed that IKKi deficiency induced cardiac hypertrophy through the activation of the AKT and NF-kB signaling pathway in response to aortic banding (AB). Non-coding RNAs, mainly long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), play a crucial role in normal developmental and pathological processes. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.014DOI Listing
February 2019
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4.882 Impact Factor

The power of metabolism - Linking energy supply and demand with cardiac contractile function.

Biochim Biophys Acta Mol Basis Dis 2019 Apr 18;1865(4):725-727. Epub 2019 Feb 18.

Maastricht University, Maastricht, the Netherlands. Electronic address:

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http://dx.doi.org/10.1016/j.bbadis.2019.02.006DOI Listing

Sequence- and seed-structure-dependent polymorphic fibrils of alpha-synuclein.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 18. Epub 2019 Feb 18.

Laboratory of Structural Neuropathology, Doshisha University Graduate School of Brain Science, 1-3 Miyakodanitatara, Kyotanabe-shi, Kyoto 610-0394, Japan. Electronic address:

Synucleinopathies comprise a diverse group of neurodegenerative diseases including Parkinson's disease (PD), dementia with Lewy bodies, and multiple system atrophy. These share a common pathological feature, the deposition of alpha-synuclein (a-syn) in neurons or oligodendroglia. A-syn is highly conserved in vertebrates, but the primary sequence of mouse a-syn differs from that of human at seven positions. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.013DOI Listing
February 2019

RhoC/ROCK2 promotes vasculogenic mimicry formation primarily through ERK/MMPs in hepatocellular carcinoma.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 16. Epub 2019 Feb 16.

Department of Clinical Pharmacy, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No.100 Haining Road, Shanghai 200080, PR China. Electronic address:

Vasculogenic mimicry (VM) results in the formation of an alternative circulatory system that can improve the blood supply to multiple malignant tumors, including hepatocellular carcinoma (HCC). However, the potential mechanisms of RhoC/ROCK in VM have not yet been investigated in HCC. Here, RhoC expression was upregulated in HCC tissues, especially the VM-positive (VM+) group, compared to noncancerous tissues (P < 0. Read More

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http://dx.doi.org/10.1016/j.bbadis.2018.12.007DOI Listing
February 2019
2 Reads
4.882 Impact Factor

Inhibition of PRMT3 activity reduces hepatic steatosis without altering atherosclerosis susceptibility in apoE knockout mice.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 15. Epub 2019 Feb 15.

Division of BioTherapeutics, Leiden Academic Centre for Drug Research, Gorlaeus Laboratories, Einsteinweg 55, 2333CC Leiden, the Netherlands.

The nuclear receptor liver X receptor (LXR) impacts on cholesterol metabolism as well as hepatic lipogenesis via transcriptional regulation. It is proposed that inhibition of the protein arginine methyltransferase 3 (PRMT3) uncouples these two transcriptional pathways in vivo by acting as a specific lipogenic coactivator of LXR. Here we validated the hypothesis that treatment with the allosteric PRMT3 inhibitor SGC707 will diminish the hepatic steatosis extent, while leaving global cholesterol metabolism, important in cholesterol-driven pathologies like atherosclerosis, untouched. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.012DOI Listing
February 2019
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The potential contribution of stromal cell-derived factor 2 (SDF2) in endoplasmic reticulum stress response in severe preeclampsia and labor-onset.

Biochim Biophys Acta Mol Basis Dis 2019 Feb 15. Epub 2019 Feb 15.

Institute of Biomedical Sciences, Department of Cell and Developmental Biology, University of São Paulo, São Paulo, SP, Brazil. Electronic address:

Endoplasmic reticulum (ER) stress occurs when the protein folding machinery in the cell is unable to cope with newly synthesized proteins, which results in an accumulation of misfolded proteins in the ER lumen. In response, the cell activates a cellular signaling pathway known as the Unfolded Protein Response (UPR), aiming to restore cellular homeostasis. Activation and exacerbation of the UPR have been described in several human pathologies, including cancer and neurological disorders, and in some gestational diseases such as preeclampsia and gestational diabetes. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.01.012DOI Listing
February 2019

FMRpolyG alters mitochondrial transcripts level and respiratory chain complex assembly in Fragile X associated tremor/ataxia syndrome [FXTAS].

Biochim Biophys Acta Mol Basis Dis 2019 Feb 13. Epub 2019 Feb 13.

Department of Biochemistry, Faculty of Science, The M.S. University of Baroda, Vadodara 390002, Gujarat, India. Electronic address:

Fragile X-associated tremor/ataxia syndrome (FXTAS) is an inherited neurodegenerative disorder caused by an expansion of 55 to 200 CGG repeats (premutation) in FMR1. These CGG repeats are Repeat Associated non-ATG (RAN) translated into a small and pathogenic protein, FMRpolyG. The cellular and molecular mechanisms of FMRpolyG toxicity are unclear. Read More

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http://dx.doi.org/10.1016/j.bbadis.2019.02.010DOI Listing
February 2019
1 Read
4.882 Impact Factor