633 results match your criteria Cellular and molecular gastroenterology and hepatology[Journal]


Proline rich acidic protein-1 (PRAP1) protects the gastrointestinal epithelium from irradiation-induced apoptosis.

Cell Mol Gastroenterol Hepatol 2020 Jul 3. Epub 2020 Jul 3.

Department of Pathology & Laboratory Medicine, Emory University, Atlanta, GA; Emory Microbiome Research Center, Emory University School of Medicine, Atlanta, USA. Electronic address:

Background & Aims: The intestinal epithelium must be resilient to physiochemical stress in order to uphold the physiological barrier separating the systemic compartment from the microbial and antigenic components of the gut lumen. Identifying proteins that mediate protection and enhancing their expression is therefore a clear approach to promote intestinal health. We previously reported that oral ingestion of the probiotic Lactobacillus rhamnosus GG (LGG) not only induced the expression of several recognized cytoprotective factors in the murine colon, but also many genes with no previously described function, including the gene encoding proline rich acidic protein-1 (PRAP1). Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.011DOI Listing

Helminth-induced and Th2-dependent alterations of the gut microbiota attenuate obesity caused by high fat diet.

Cell Mol Gastroenterol Hepatol 2020 Jul 3. Epub 2020 Jul 3.

Mucosal Immunology and Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, USA. Electronic address:

Background & Aims: Epidemiological and animal studies have indicated an inverse correlation between the rising prevalence of obesity and metabolic syndrome and exposure to helminths. Whether helminth-induced immune response contributes to microbiota remodeling in obesity remains unknown. The aim of this study is to explore the immune-regulatory role of helminth in the prevention of HFD-induced obesity through remodeling gut microbiome. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.010DOI Listing

LLGL1 regulates gemcitabine resistance by modulating ERK-SP1-OSMR pathway in pancreatic ductal adenocarcinoma.

Cell Mol Gastroenterol Hepatol 2020 Jun 29. Epub 2020 Jun 29.

School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong; Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen 518087, China. Electronic address:

Background & Aims: Gemcitabine resistance is rapidly acquired by pancreatic ductal adenocarcinoma (PDAC) patients. Novel approaches that predict gemcitabine response of patients and enhance gemcitabine chemosensitivity are important to improve patients' survival. We aimed to identify genes as novel biomarkers to predict gemcitabine response and the therapeutic targets to attenuate chemoresistance in PDAC cells. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.009DOI Listing

Nature or Nurture? The Answer Is "Both" in Nonalcoholic Steatohepatitis.

Authors:
Rotonya M Carr

Cell Mol Gastroenterol Hepatol 2020 Jun 29. Epub 2020 Jun 29.

University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.003DOI Listing

Mystery Solving: Acid Reflux and Cell Mobility in Barrett's Esophagus and Esophageal Adenocarcinoma.

Cell Mol Gastroenterol Hepatol 2020 Jun 26. Epub 2020 Jun 26.

University of Houston, Houston, Texas.

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.002DOI Listing

Mitochondrial Networks: A New Therapeutic Target in Colitis.

Authors:
Lee A Denson

Cell Mol Gastroenterol Hepatol 2020 Jun 24. Epub 2020 Jun 24.

Pediatric Gastroenterology, Hepatology, and Nutrition, University of Cincinnati College of Medicine and, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.008DOI Listing

Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Epithelial Barrier Integrity in Patients With Crohn's Disease.

Cell Mol Gastroenterol Hepatol 2020 Jun 16. Epub 2020 Jun 16.

Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Electronic address:

Background & Aims: Intestinal epithelial cell (IEC) barrier dysfunction is critical to the development of Crohn's disease (CD). However, the mechanism is understudied. We recently reported increased microRNA-31-5p (miR-31-5p) expression in colonic IECs of CD patients, but downstream targets and functional consequences are unknown. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.005DOI Listing

Acetyl-CoA Carboxylase Inhibition Improves Multiple Dimensions of NASH Pathogenesis in Model Systems.

Cell Mol Gastroenterol Hepatol 2020 Jun 9. Epub 2020 Jun 9.

Internal Medicine Research Unit, Pfizer Worldwide Research and Development, Cambridge Massachusetts. Electronic address:

Background & Aims: Disordered metabolism, steatosis, hepatic inflammation, and fibrosis contribute to the pathogenesis of nonalcoholic steatohepatitis (NASH). Acetyl-CoA carboxylase (ACC) catalyzes the first committed step in de novo lipogenesis (DNL) and modulates mitochondrial fatty acid oxidation. Increased hepatic DNL flux and reduced fatty acid oxidation are hypothesized to contribute to steatosis. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.06.001DOI Listing

Mechanistic Understanding of the Symbiotic Relationship Between the Gut Microbiota and the Host: An Avenue Toward Therapeutic Applications.

Authors:
Fang Yan

Cell Mol Gastroenterol Hepatol 2020 Jun 8. Epub 2020 Jun 8.

Division of Gastroenterology, Hepatology & Nutrition, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.003DOI Listing

Insulin-like Growth Factor-1 and mTORC1 Signaling Promote the Intestinal Regenerative Response After Irradiation Injury.

Cell Mol Gastroenterol Hepatol 2020 Jun 2. Epub 2020 Jun 2.

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan; Cellular and Molecular Biology Graduate Program, University of Michigan, Ann Arbor, Michigan. Electronic address:

Background & Aims: Intestinal crypts have a remarkable capacity to regenerate after injury from loss of crypt base columnar (CBC) stem cells. After injury, facultative stem cells (FSCs) are activated to replenish the epithelium and replace lost CBCs. Our aim was to assess the role of insulin-like growth factor-1 (IGF-1) to activate FSCs for crypt repair. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.013DOI Listing

A Nucleotide Analog Prevents Colitis-Associated Cancer via Beta-Catenin Independently of Inflammation and Autophagy.

Cell Mol Gastroenterol Hepatol 2020 Jun 1. Epub 2020 Jun 1.

Inflammatory Bowel Diseases Group, Mater Research Institute - University of Queensland, Translational Research Institute, Woolloongabba, Queensland; Inflammatory Disease Biology and Therapeutics Group, Mater Research Institute - University of Queensland, Translational Research Institute, Woolloongabba, Queensland; School of Medicine, Faculty of Medicine, University of Queensland. Electronic address:

Background & Aims: Chronic bowel inflammation increases the risk of colon cancer, colitis-associated cancer (CAC). Thiopurine use is associated with a reduction in dysplasia and CAC in inflammatory bowel disease (IBD). Abnormal Wnt/β-catenin signalling is characteristic of >90% of colorectal cancers. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.012DOI Listing

Vitamin D Receptor Protects Against Dysbiosis and Tumorigenesis via the JAK/STAT Pathway in Intestine.

Cell Mol Gastroenterol Hepatol 2020 Jun 1. Epub 2020 Jun 1.

Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois; UIC Cancer Center, University of Illinois at Chicago, Chicago, Illinois. Electronic address:

Background & Aims: Vitamin D exerts regulatory roles via vitamin D receptor (VDR) in mucosal immunity, host defense, and inflammation involving host factors and microbiome. Human Vdr gene variation shapes the microbiome and VDR deletion leads to dysbiosis. Low VDR expression and diminished vitamin D/VDR signaling are observed in colon cancer. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.010DOI Listing

Towards a Comprehensive Understanding of Human Norovirus Immunity.

Authors:
Vesselin Tomov

Cell Mol Gastroenterol Hepatol 2020 May 29. Epub 2020 May 29.

University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.019DOI Listing

The Hidden Effect of Nod2 in the Host/Microbiota Relationship.

Cell Mol Gastroenterol Hepatol 2020 May 29. Epub 2020 May 29.

INSERM, U1016, Team "Mucosal Microbiota in Chronic Inflammatory Diseases", Paris, France; Université de Paris, Paris, France; Institute for Biomedical Sciences, Center for Inflammation, Immunity and Infection, Georgia State University, Atlanta, Georgia; Neuroscience Institute, Georgia State University, Atlanta, Georgia. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.001DOI Listing

IL23 Promotes Antimicrobial Pathways in Human Macrophages, Which Are Reduced With the IBD-Protective IL23R R381Q Variant.

Cell Mol Gastroenterol Hepatol 2020 May 29. Epub 2020 May 29.

Section of Digestive Diseases, Department of Internal Medicine, Yale University, New Haven, Connecticut. Electronic address:

Background & Aims: Interleukin (IL)23 is a major contributor to inflammatory bowel disease (IBD) pathogenesis and is being pursued as a therapeutic target, both through targeting IL23 alone or in combination with IL12. Unexpected trial outcomes highlight the importance of understanding the cell types through which IL23 regulates immune responses, and how IL23 and IL12 compare in these responses. Macrophages are key players in IBD, and IL23 recently was found to promote inflammatory outcomes in human macrophages. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.007DOI Listing

The EXTrauterine Environment for Neonatal Development Supports Normal Intestinal Maturation and Development.

Cell Mol Gastroenterol Hepatol 2020 May 28. Epub 2020 May 28.

Children's Hospital of Philadelphia Research Institute, Philadelphia, Pennsylvania; Department of Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address:

Background And Aims: The Extra-Uterine Environment for Neonatal Development (EXTEND) aims to avoid the complications of prematurity, such as NEC. Our goal was to determine if bowel development occurs normally in EXTEND-supported lambs, with specific emphasis on markers of immaturity associated with NEC.

Methods: We compared terminal ileum from 17 pre-term lambs supported on EXTEND for 2- 4 weeks to bowel from age-matched fetal lambs that developed in utero. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.006DOI Listing

Sirtuin-6 in Hepatic Fibrosis: Does Cell Type Matter?

Cell Mol Gastroenterol Hepatol 2020 May 29. Epub 2020 May 29.

Vascular Medicine Institute, Department of Medicine, Pittsburgh Liver Research Center, University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.017DOI Listing

The Villin1 Gene Promoter Drives Cre Recombinase Expression in Extraintestinal Tissues.

Cell Mol Gastroenterol Hepatol 2020 May 25. Epub 2020 May 25.

Division of Gastroenterology, Hepatology and Nutrition, Boston Children's Hospital, Boston, Massachusetts; Department of Pediatrics, Harvard Medical School, Boston, Massachusetts. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.009DOI Listing

Differential Contribution of Pancreatic Fibroblast Subsets to the Pancreatic Cancer Stroma.

Cell Mol Gastroenterol Hepatol 2020 May 23. Epub 2020 May 23.

Department of Surgery; Rogel Cancer Center; Department of Cell and Developmental Biology. Electronic address:

Background & Aims: Although the healthy pancreas consists mostly of epithelial cells, pancreatic cancer and the precursor lesions known as pancreatic intraepithelial neoplasia, are characterized by an extensive accumulation of fibroinflammatory stroma that includes a substantial and heterogeneous fibroblast population. The cellular origin of fibroblasts within the stroma has not been determined. Here, we show that the Gli1 and Hoxb6 markers label distinct fibroblast populations in the healthy mouse pancreas. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.004DOI Listing

GIPC-Regulated IGFBP-3 Promotes HSC Migration In Vitro and Portal Hypertension In Vivo Through a β1-Integrin Pathway.

Cell Mol Gastroenterol Hepatol 2020 May 22. Epub 2020 May 22.

Gastroenterology Research Unit, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. Electronic address:

Background & Aims: Transforming growth factor (TGF-β)-induced activation of quiescent hepatic stellate cells (HSCs) and their transformation to myofibroblasts is a key event in liver fibrosis and portal hypertension. GIPC (also referred to as synectin) is a downstream signal activation molecule of TGF-β and other receptors. In this study, we sought to identify novel genes targeted by TGF-β and GIPC and elucidate if and how they may contribute to liver fibrosis. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.005DOI Listing

High Content Imaging of Barrett's-Associated High-Grade Dysplasia Cells After siRNA Library Screening Reveals Acid-Responsive Regulators of Cellular Transitions.

Cell Mol Gastroenterol Hepatol 2020 May 13. Epub 2020 May 13.

Life Science Institute, University of British Columbia, Vancouver, British Columbia, Canada; Division of Gastroenterology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Centre for Complement and Inflammation Research, Imperial College London, London, United Kingdom. Electronic address:

Background & Aims: Esophageal adenocarcinoma (EAC) develops from within Barrett's esophagus (BE) concomitant with gastroesophageal reflux disease (GERD). Wound healing processes and cellular transitions, such as epithelial-mesenchymal transitions, may contribute to the development of BE and the eventual migratory escape of metastatic cancer cells. Herein, we attempt to identify the genes underlying esophageal cellular transitions and their potential regulation by the low pH environments observed in GERD and commonly encountered by escaping cancer cells. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.05.002DOI Listing

Inhibition of Microglial Activation in the Amygdala Reverses Stress-Induced Abdominal Pain in the Male Rat.

Cell Mol Gastroenterol Hepatol 2020 May 8. Epub 2020 May 8.

Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Oklahoma City VA Health Care System, Oklahoma City, Oklahoma; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. Electronic address:

Background & Aims: Psychological stress is a trigger for the development of irritable bowel syndrome and associated symptoms including abdominal pain. Although irritable bowel syndrome patients show increased activation in the limbic brain, including the amygdala, the underlying molecular and cellular mechanisms regulating visceral nociception in the central nervous system are incompletely understood. In a rodent model of chronic stress, we explored the role of microglia in the central nucleus of the amygdala (CeA) in controlling visceral sensitivity. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.020DOI Listing

Alternative Splicing in Hepatocellular Carcinoma.

Cell Mol Gastroenterol Hepatol 2020 May 8. Epub 2020 May 8.

Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. Electronic address:

Hepatocellular carcinoma (HCC) accounts for the majority of primary liver cancer cases, with more than 850,000 new diagnoses per year globally. Recent trends in the United States have shown that liver cancer mortality has continued to increase in both men and women, while 5-year survival remains less than 20%. Understanding key mechanisms that drive chronic liver disease progression to HCC can show new therapeutic targets and biomarkers for early detection of HCC. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.018DOI Listing

Norepinephrine Has Dual Effects on Human Colonic Contractions Through Distinct Subtypes of Alpha 1 Adrenoceptors.

Cell Mol Gastroenterol Hepatol 2020 May 4. Epub 2020 May 4.

Department of Cell Physiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.

Background & Aims: Colonic musculature contain smooth muscle cells (SMC), interstitial cells of Cajal (ICC), and platelet-derived growth factor receptor α cells (PDGFRα cells), which are electrically coupled and operate together as the SIP syncytium. PDGFRα cells have enriched expression of small conductance Ca-activated K (SK) channels. Purinergic enteric neural input activates SK channels in PDGFRα cells, hyperpolarizes SMC, and inhibits colonic contractions. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.015DOI Listing

Interleukin 27 Protects From Gastric Atrophy and Metaplasia During Chronic Autoimmune Gastritis.

Cell Mol Gastroenterol Hepatol 2020 May 4. Epub 2020 May 4.

Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri. Electronic address:

Background & Aims: The association between chronic inflammation and gastric carcinogenesis is well established, but it is not clear how immune cells and cytokines regulate this process. We investigated the role of interleukin 27 (IL27) in the development of gastric atrophy, hyperplasia, and metaplasia (preneoplastic lesions associated with inflammation-induced gastric cancer) in mice with autoimmune gastritis.

Methods: We performed studies with TxA23 mice (control mice), which express a T-cell receptor against the H+/K+ adenosine triphosphatase α chain and develop autoimmune gastritis, and TxA23xEbi3 mice, which develop gastritis but do not express IL27. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.014DOI Listing

Pharmacologic Activation of the G Protein-Coupled Estrogen Receptor Inhibits Pancreatic Ductal Adenocarcinoma.

Cell Mol Gastroenterol Hepatol 2020 May 4. Epub 2020 May 4.

Perelman School of Medicine, Department of Dermatology, University of Pennsylvania, Philadelphia.

Background & Aims: Female sex is associated with lower incidence and improved clinical outcomes for most cancer types including pancreatic ductal adenocarcinoma (PDAC). The mechanistic basis for this sex difference is unknown. We hypothesized that estrogen signaling may be responsible, despite the fact that PDAC lacks classic nuclear estrogen receptors. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.016DOI Listing

Escherichia coli-Specific CD4+ T Cells Have Public T-Cell Receptors and Low Interleukin 10 Production in Crohn's Disease.

Cell Mol Gastroenterol Hepatol 2020 May 1. Epub 2020 May 1.

Benroya Research Institute, Seattle, Washington; Virginia Mason Medical Center, Seattle, Washington. Electronic address:

Background & Aims: Crohn's disease (CD) likely represents decreased immune tolerance to intestinal bacterial antigens. Most CD patients have high titers of antibodies to intestinal commensal proteins, including the outer membrane porin C (OmpC) of Escherichia coli.

Methods: By using major histocompatibility complex II tetramers, we identified an HLA-DRB1∗15:01-restricted peptide epitope of OmpC recognized by CD4+ T cells in peripheral blood mononuclear cells from HLA-DRB1∗15:01+ healthy control (HC) and CD patients. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.013DOI Listing

Tamoxifen Acts as a Parietal Cell Protonophore.

Cell Mol Gastroenterol Hepatol 2020 Apr 30. Epub 2020 Apr 30.

Department of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, Tennessee; Nashville VA Medical Center, Nashville, Tennessee; Department of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.012DOI Listing

Diet Reversal and Immune Modulation Show Key Role for Liver and Adipose Tissue T Cells in Murine Nonalcoholic Steatohepatitis.

Cell Mol Gastroenterol Hepatol 2020 Apr 29. Epub 2020 Apr 29.

Translational Research in Immunology and Inflammation, Laboratory of Experimental Medicine and Pediatrics, Division of Gastroenterology and Hepatology, University of Antwerp, Antwerp, Belgium; Department of Gastroenterology and Hepatology, Antwerp University Hospital, Edegem, Belgium; Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium.

Background & Aims: Nonalcoholic steatohepatitis (NASH) is a multisystem condition, implicating liver and adipose tissue. Although the general involvement of the innate and adaptive immune system has been established, we aimed to define the exact role of the functionally diverse T-cell subsets in NASH pathogenesis through diet reversal and immunologic modulation.

Methods: Multiple experimental set-ups were used in 8-week-old C57BL/6J mice, including prolonged high-fat high-fructose diet (HFHFD) feeding, diet reversal from HFHFD to control diet, and administration of anti-CD8a and anti-interleukin 17A antibodies. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.010DOI Listing

Incapacitated Capicua in Sorafenib-Resistant HCC.

Cell Mol Gastroenterol Hepatol 2020 Apr 27. Epub 2020 Apr 27.

Division of Gastroenterology, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.007DOI Listing

Genome-Scale Analysis Identifies Novel Transcript-Variants in Esophageal Adenocarcinoma.

Cell Mol Gastroenterol Hepatol 2020 Apr 25. Epub 2020 Apr 25.

Division of General Medical Sciences-Oncology, Case Western Reserve University School of Medicine, Cleveland, Ohio; Department of Pathology, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.011DOI Listing

Are Wnt/β-Catenin and PI3K/AKT/mTORC1 Distinct Pathways in Colorectal Cancer?

Cell Mol Gastroenterol Hepatol 2020 Apr 22. Epub 2020 Apr 22.

Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy; Center for Applied Biomedical Research, S. Orsola Hospital, University of Bologna, Bologna, Italy. Electronic address:

Wnt/β-catenin and phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin complex 1 (PI3K/AKT/mTORC1) pathways both are critically involved in colorectal cancer (CRC) development, although they are implicated in the modulation of distinct oncogenic mechanisms. In homeostatic and pathologic conditions, these pathways show a fine regulation based mainly on feedback mechanisms, and are connected at multiple levels involving both upstream and downstream common effectors. The ability of the Wnt/β-catenin and PI3K/AKT/mTORC1 pathways to reciprocally control themselves represents one of the main resistance mechanisms to selective inhibitors in CRC, leading to the hypothesis that in specific settings, particularly in cancer driven by genetic alterations in Wnt/β-catenin signaling, the relationship between Wnt/β-catenin and PI3K/AKT/mTORC1 pathways could be so close that they should be considered as a unique therapeutic target. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.007DOI Listing

Hypergastrinemia Expands Gastric ECL Cells Through CCK2R Progenitor Cells via ERK Activation.

Cell Mol Gastroenterol Hepatol 2020 Apr 21. Epub 2020 Apr 21.

Division of Digestive and Liver Diseases, Department of Medicine. Electronic address:

Background & Aims: Enterochromaffin-like (ECL) cells in the stomach express gastrin/cholecystokinin 2 receptor CCK2R and are known to expand under hypergastrinemia, but whether this results from expansion of existing ECL cells or increased production from progenitors has not been clarified.

Methods: We used mice with green fluorescent protein fluorescent reporter expression in ECL cells (histidine decarboxylase [Hdc]-green fluorescent protein), as well as Cck2r- and Hdc-driven Tamoxifen inducible recombinase Cre (Cck2r-CreERT2, Hdc-CreERT2) mice combined with Rosa26Sor-tdTomato (R26-tdTomato) mice, and studied their expression and cell fate in the gastric corpus by using models of hypergastrinemia (gastrin infusion, omeprazole treatment).

Results: Hdc-GFP marked the majority of ECL cells, located in the lower third of the gastric glands. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.008DOI Listing

Inhibition of Hepatic Bile Acid Uptake by Myrcludex B Promotes Glucagon-Like Peptide-1 Release and Reduces Obesity.

Cell Mol Gastroenterol Hepatol 2020 Apr 21. Epub 2020 Apr 21.

Tytgat Institute for Liver and Intestinal Research, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Department of Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, the Netherlands. Electronic address:

Background & Aims: Bile acids are important metabolic signaling molecules. Bile acid receptor activation promotes body weight loss and improves glycemic control. The incretin hormone GLP-1 and thyroid hormone activation of T4 to T3 have been suggested as important contributors. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.009DOI Listing

A Central Role for Lipocalin-2 in the Adaptation to Short-Bowel Syndrome Through Down-Regulation of IL22 in Mice.

Cell Mol Gastroenterol Hepatol 2020 Apr 21;10(2):309-326. Epub 2020 Apr 21.

Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland. Electronic address:

Background & Aims: In short-bowel syndrome (SBS), inadequate intestinal adaptation is responsible for the majority of complications, including sepsis, liver failure, and death. In this study, we sought to further delineate the adaptive response to identify potential therapeutic targets.

Methods: We performed a 75% small-bowel resection (SBR) or sham operation on C57Bl/6J wild-type (WT), lipocalin-2 (LCN2), and interleukin 22 (IL22) mice. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327842PMC

SIRT6 Protects Against Liver Fibrosis by Deacetylation and Suppression of SMAD3 in Hepatic Stellate Cells.

Cell Mol Gastroenterol Hepatol 2020 Apr 17;10(2):341-364. Epub 2020 Apr 17.

Department of Biochemistry and Molecular Biology; Center for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address:

Background & Aims: Nonalcoholic steatohepatitis (NASH) is a chronic liver disease that is manifested clinically by an increase in hepatic triglycerides, inflammation, and fibrosis. The pathogenesis of NASH remains incompletely understood. Sirtuin 6 (Sirt6), a nicotinamide adenine dinucleotide-dependent deacetylase, has been implicated in fatty liver disease; however, the underlying molecular mechanisms in the NASH pathogenesis are elusive. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327931PMC

Tight Junctions as Targets and Effectors of Mucosal Immune Homeostasis.

Cell Mol Gastroenterol Hepatol 2020 Apr 15;10(2):327-340. Epub 2020 Apr 15.

Laboratory of Mucosal Barrier Pathophysiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Electronic address:

Defective epithelial barrier function is present in maladies including epidermal burn injury, environmental lung damage, renal tubular disease, and a range of immune-mediated and infectious intestinal disorders. When the epithelial surface is intact, the paracellular pathway between cells is sealed by the tight junction. However, permeability of tight junctions varies widely across tissues and can be markedly impacted by disease. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326733PMC

Characterization of a p53/miR-34a/CSF1R/STAT3 Feedback Loop in Colorectal Cancer.

Cell Mol Gastroenterol Hepatol 2020 Apr 15;10(2):391-418. Epub 2020 Apr 15.

Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-University Munich, Munich, Germany; German Cancer Consortium, Partner site Munich, Munich, Germany; German Cancer Research Center, Heidelberg, Germany. Electronic address:

Background & Aims: The miR-34a gene is a direct target of p53 and is commonly silenced in colorectal cancer (CRC). Here we identified the receptor tyrosine kinase CSF1R as a direct miR-34a target and characterized CSF1R as an effector of p53/miR-34a-mediated CRC suppression.

Methods: Analyses of TCGA-COAD and three other CRC cohorts for association of mRNA expression and signatures with patient survival and molecular subtypes. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.002DOI Listing

Perturbed Mitochondrial Dynamics Is a Novel Feature of Colitis That Can Be Targeted to Lessen Disease.

Cell Mol Gastroenterol Hepatol 2020 Apr 13;10(2):287-307. Epub 2020 Apr 13.

Gastrointestinal Research Group (GIRG) and Inflammation Research Network, Department of Physiology and Pharmacology, Calvin, Joan and Phoebe Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary. Electronic address:

Background & Aims: Mitochondria exist in a constantly remodelling network, and excessive fragmentation can be pathophysiological. Mitochondrial dysfunction can accompany enteric inflammation, but any contribution of altered mitochondrial dynamics (ie, fission/fusion) to gut inflammation is unknown. We hypothesized that perturbed mitochondrial dynamics would contribute to colitis. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327843PMC

Virus-Host Interactions Between Nonsecretors and Human Norovirus.

Cell Mol Gastroenterol Hepatol 2020 Apr 11;10(2):245-267. Epub 2020 Apr 11.

Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina. Electronic address:

Background & Aims: Human norovirus infection is the leading cause of acute gastroenteritis. Genetic polymorphisms, mediated by the FUT2 gene (secretor enzyme), define strain susceptibility. Secretors express a diverse set of fucosylated histoblood group antigen carbohydrates (HBGA) on mucosal cells; nonsecretors (FUT2) express a limited array of HBGAs. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301201PMC

Colitis-Induced Microbial Perturbation Promotes Postinflammatory Visceral Hypersensitivity.

Cell Mol Gastroenterol Hepatol 2020 Apr 11;10(2):225-244. Epub 2020 Apr 11.

Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Division of Gastroenterology and Hepatology, Department of Medicine, University of Calgary. Electronic address:

Background & Aims: Despite achieving endoscopic remission, more than 20% of inflammatory bowel disease patients experience chronic abdominal pain. These patients have increased rectal transient receptor potential vanilloid-1 receptor (TRPV1) expression, a key transducer of inflammatory pain. Because inflammatory bowel disease patients in remission exhibit dysbiosis and microbial manipulation alters TRPV1 function, our goal was to examine whether microbial perturbation modulated transient receptor potential function in a mouse model. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.04.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301239PMC

NOD2 Influences Trajectories of Intestinal Microbiota Recovery After Antibiotic Perturbation.

Cell Mol Gastroenterol Hepatol 2020 Apr 11;10(2):365-389. Epub 2020 Apr 11.

Institute of Clinical Molecular Biology, Kiel, Germany. Electronic address:

Background & Aims: Loss-of-function variants in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) impair the recognition of the bacterial cell wall component muramyl-dipeptide and are associated with an increased risk for developing Crohn's disease. Likewise, exposure to antibiotics increases the individual risk for developing inflammatory bowel disease. Here, we studied the long-term impact of NOD2 on the ability of the gut bacterial and fungal microbiota to recover after antibiotic treatment. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327897PMC

Quantifying the Complexities of Bile Acid Metabolism in Man: Continued Progress.

Authors:
Alan F Hofmann

Cell Mol Gastroenterol Hepatol 2020 30;10(1):201-202. Epub 2020 Mar 30.

Department of Medicine, University of California, San Diego, La Jolla, California. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296227PMC

Protein Kinase D1 (PKD1) Signaling Induces Growth-Promoting Effects in Murine Enteroids.

Cell Mol Gastroenterol Hepatol 2020 Mar 28. Epub 2020 Mar 28.

Department of Medicine, Los Angeles, California; Department of Pediatrics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California; CURE: Digestive Diseases Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.005DOI Listing

Alcohol-Induced Pancreatitis: A Critical Role for TFEB in Maintaining Lysosomal Biogenesis and Autophagic Clearance.

Cell Mol Gastroenterol Hepatol 2020 26;10(1):199-200. Epub 2020 Mar 26.

Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296224PMC

Here to Heal: Mucosal CD74 Signaling in Colitis.

Cell Mol Gastroenterol Hepatol 2020 24;10(1):197-198. Epub 2020 Mar 24.

Center for Inflammatory Bowel Diseases, Vatche and Tamar Manoukian, Division of Digestive Diseases, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296222PMC

Glutamine Breakdown as a Potential Metabolic Biomarker for Nonalcoholic Steatohepatitis.

Cell Mol Gastroenterol Hepatol 2020 24;10(1):195-196. Epub 2020 Mar 24.

Department of Physiology, Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.03.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296225PMC

Inactivation of Transcriptional Repressor Capicua Confers Sorafenib Resistance in Human Hepatocellular Carcinoma.

Cell Mol Gastroenterol Hepatol 2020 Mar 10;10(2):269-285. Epub 2020 Mar 10.

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Ishikawa 920-8641, Japan.

Background & Aims: Sorafenib is a multireceptor tyrosine kinase inhibitor that can prolong overall survival in patients with advanced hepatocellular carcinoma (HCC). Although most HCC patients who receive sorafenib ultimately show disease progression, it still is unclear whether and how HCC cells acquire chemoresistance during sorafenib treatment in human beings.

Methods: We analyzed surgically resected HCC tissues from a patient who received sorafenib for prevention of HCC recurrence after surgery (Adjuvant Sorafenib for Hepatocellular Carcinoma after Resection or Ablation trial) and established patient-derived HCC cells. Read More

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http://dx.doi.org/10.1016/j.jcmgh.2020.02.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305345PMC

Inflammasome-more Injury in Cholestasis.

Cell Mol Gastroenterol Hepatol 2020 7;9(4):711-712. Epub 2020 Mar 7.

Division of Gastroenterology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.02.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212471PMC

Intracellular Control of β-Catenin and Intestinal Cell Fate by SIRT2.

Authors:
Mark R Frey

Cell Mol Gastroenterol Hepatol 2020 6;10(1):193-194. Epub 2020 Mar 6.

Saban Research Institute, Children's Hospital Los Angeles, Los Angeles, California; Department of Pediatrics and Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles, California. Electronic address:

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http://dx.doi.org/10.1016/j.jcmgh.2020.02.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7296226PMC