4,054 results match your criteria enos activation

New Therapeutic Insight into the Effect of Ma Huang Tang on Blood Pressure and Renal Dysfunction in the L-NAME-Induced Hypertension.

Evid Based Complement Alternat Med 2021 13;2021:9980429. Epub 2021 Jul 13.

Hanbang Cardio-Renal Syndrome Research Center, Wonkwang University, 460 Iksan-daero, Iksan, Jeonbuk 54538, Republic of Korea.

In this study, we evaluated the effect of a traditional herbal formula, Ma Huang Tang (MHT), on blood pressure and vasodilation in a rat model of N-nitro-L-arginine methylester- (L-NAME-) induced hypertension. We found that MHT-induced vascular relaxation in a dose-dependent manner in rat aortas pretreated with phenylephrine. However, pretreatment of endothelium-intact aortic rings with L-NAME, an inhibitor of nitric oxide synthesis (NOS), or 1H-[1, 2, 4]-oxadiazole-[4, 3-]-quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, significantly abolished vascular relaxation induced by MHT. Read More

View Article and Full-Text PDF

Activation of κ-opioid receptor inhibits inflammatory response induced by sodium palmitate in human umbilical vein endothelial cells.

Cytokine 2021 Jul 28;146:155659. Epub 2021 Jul 28.

Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, Air Force Medical University, No. 169 West Changle Road, Xi'an 710032, Shaanxi Province, People's Republic of China; School of Life Sciences, Northwest University, No.1 North Taibai Road, Xi'an 710069, Shaanxi Province, People's Republic of China. Electronic address:

Objectives: The current study aims to investigate the effect of κ-opioid receptor (κ-OR) activation on sodium palmitate (SP)-induced human umbilical vein endothelial cells (HUVECs) inflammatory response and elucidate the underlying mechanisms.

Methods: A hyperlipidemic cell model was established and treated with κ-OR agonist (U50,488H), and antagonist (norbinaltorphimine, nor-BNI), or inhibitors targeting PI3K, Akt or eNOS (LY294002, MK2206-2HCl or L-NAME, respectively). Furthermore, the expression levels of NLRP3, caspase-1, p-Akt, Akt, p-eNOS, and total eNOS were evaluated. Read More

View Article and Full-Text PDF

Multiple Inducers of endothelial NOS (eNOS) Dysfunction in Sickle Cell Disease.

Am J Hematol 2021 Jul 31. Epub 2021 Jul 31.

Division of Hematology-Oncology-Transplantation, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA.

A characteristic aspect of the robust, systemic inflammatory state in sickle cell disease is dysfunction of endothelial nitric oxide synthase (eNOS). We identify ten aberrant endothelial cell inputs, present in the specific sickle context, that are known to have the ability to cause eNOS dysfunction. These are: endothelial arginase depletion, asymmetric dimethylarginine, complement activation, endothelial glycocalyx degradation, free fatty acids, inflammatory mediators, microparticles, oxidized low density lipoproteins, reactive oxygen species, and Toll-like receptor 4 signaling ligands. Read More

View Article and Full-Text PDF

Exercise training mitigates ER stress and UCP2 deficiency-associated coronary vascular dysfunction in atherosclerosis.

Sci Rep 2021 Jul 29;11(1):15449. Epub 2021 Jul 29.

Department of Health and Human Performance, Laboratory of Integrated Physiology, University of Houston, 3875 Holman St, Houston, TX, 77204-6015, USA.

Endoplasmic reticulum (ER) stress and uncoupling protein-2 (UCP2) activation are opposing modulators of endothelial dysfunction in atherosclerosis. Exercise reduces atherosclerosis plaques and enhances endothelial function. Our aim was to understand how exercise affects ER stress and UCP2 activation, and how that relates to endothelial dysfunction in an atherosclerotic murine model. Read More

View Article and Full-Text PDF

Crambescin C1 Acts as A Possible Substrate of iNOS and eNOS Increasing Nitric Oxide Production and Inducing Hypotensive Effect.

Front Pharmacol 2021 7;12:694639. Epub 2021 Jul 7.

Departamento de Farmacología, Facultad de Veterinaria, Universidad de Santiago de Compostela, Lugo, Spain.

Crambescins are guanidine alkaloids from the sponge . Crambescin C1 (CC) induces metallothionein genes and nitric oxide (NO) is one of the triggers. We studied and compared the , effects of some crambescine A and C analogs. Read More

View Article and Full-Text PDF

An herbal preparation ameliorates heart failure with preserved ejection fraction by alleviating microvascular endothelial inflammation and activating NO-cGMP-PKG pathway.

Phytomedicine 2021 Jun 20;91:153633. Epub 2021 Jun 20.

First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 300193, China.; Hubei Key Laboratory of Economic Forest Germplasm Improvement and Resources Comprehensive Utilization, Huanggang Normal University, Huanggang 438000, China.. Electronic address:

Background: Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous disease presenting a substantial challenge to clinicians. Currently, there is no safe and efficacious HFpEF treatment. In this study, we reported a standardized herbal medicinal product, QiShenYiQi (QSYQ), that can be used in the treatment of HFpEF. Read More

View Article and Full-Text PDF

Loss of P2Y receptor triggers glaucoma-like pathology in mice.

Br J Pharmacol 2021 Jul 26. Epub 2021 Jul 26.

Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Yamanashi, Japan.

Background And Purpose: Glaucoma, the leading cause of blindness, damages the retinal ganglion cells (RGCs). Elevated intraocular pressure (IOP) is a high-risk factor for glaucoma, so topical hypotensive drugs are usually used for treatment. However, not all patients adequately respond to current treatments, so there is a need to identify a new molecular target to reduce IOP. Read More

View Article and Full-Text PDF

PDGF-BB/SA/Dex injectable hydrogels accelerate BMSC-mediated functional full thickness skin wound repair by promoting angiogenesis.

J Mater Chem B 2021 Jul 23. Epub 2021 Jul 23.

School of Life Sciences, Zhengzhou University, 100 Science Avenue, Zhengzhou 450001, Henan, China.

Wound healing is a well-orchestrated dynamic and interactive process, which needs a favorable microenvironment and suitable angiogenesis. Platelet derived growth factor-BB (PDGF-BB) plays a crucial role in wound healing. However, the short half-life of PDGF-BB limits its efficacy. Read More

View Article and Full-Text PDF

Protein tyrosine phosphatase 1B inhibition improves endoplasmic reticulum stress‑impaired endothelial cell angiogenic response: A critical role for cell survival.

Mol Med Rep 2021 Sep 23;24(3). Epub 2021 Jul 23.

Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P.O. Box 2713 Doha, Qatar.

Endoplasmic reticulum (ER) stress contributes to endothelial dysfunction, which is the initial step in atherogenesis. Blockade of protein tyrosine phosphatase (PTP)1B, a negative regulator of insulin receptors that is critically located on the surface of ER membrane, has been found to improve endothelial dysfunction. However, the role of ER stress and its related apoptotic sub‑pathways in PTP1B‑mediated endothelial dysfunction, particularly its angiogenic capacity, have not yet been fully elucidated. Read More

View Article and Full-Text PDF
September 2021

Analysis of miRNA expression profile in lung tissues of an intermittent hypoxia rat model.

Respir Physiol Neurobiol 2021 Jul 14;294:103741. Epub 2021 Jul 14.

Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China. Electronic address:

We screened key miRNAs in an intermittent hypoxia rat model and explored the biological roles of downstream target genes and related regulatory pathways. We analyzed the expression profile of miRNAs in the lung tissues of rats in the 5 % (IH1), 7.5 % (IH2), 10 % (IH3), 12. Read More

View Article and Full-Text PDF

Exosomes derived from adipose-derived stem cells overexpressing glyoxalase-1 protect endothelial cells and enhance angiogenesis in type 2 diabetic mice with limb ischemia.

Stem Cell Res Ther 2021 07 15;12(1):403. Epub 2021 Jul 15.

Department of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200011, China.

Background: Diabetic limb ischemia is a clinical syndrome and refractory to therapy. Our previous study demonstrated that adipose-derived stem cells (ADSCs) overexpressing glyoxalase-1 (GLO-1) promoted the regeneration of ischemic lower limbs in diabetic mice, but low survival rate, difficulty in differentiation, and tumorigenicity of the transplanted cells restricted its application. Recent studies have found that exosomes secreted by the ADSCs have the advantages of containing parental beneficial factors and exhibiting non-immunogenic, non-tumorigenic, and strong stable characteristics. Read More

View Article and Full-Text PDF

The associations between THBD c.1418C>T polymorphism and lower extremity deep vein thrombosis or endothelial progenitor cell.

Int Angiol 2021 Jul 8. Epub 2021 Jul 8.

Department of General Surgery, the First People's Hospital of Yunnan Province, Kunming, Yunnan, China -

Background: Studies have shown that the thrombomodulin gene (THBD) c.1418C>T polymorphism is associated with a variety of cardiovascular diseases. However, the study of THBD c. Read More

View Article and Full-Text PDF

Distinct Signaling Functions of Rap1 Isoforms in NO Release From Endothelium.

Front Cell Dev Biol 2021 17;9:687598. Epub 2021 Jun 17.

Blood Research Institute, Versiti, Milwaukee, WI, United States.

Small GTPase Rap1 plays a prominent role in endothelial cell (EC) homeostasis by promoting NO release. Endothelial deletion of the two highly homologous Rap1 isoforms, Rap1A and Rap1B, leads to endothelial dysfunction and hypertension . Mechanistically, we showed that Rap1B promotes NO release in response to shear flow by promoting mechanosensing complex formation involving VEGFR2 and Akt activation. Read More

View Article and Full-Text PDF

The Protective Effect of Tetrahydroxystilbene Glucoside on High Glucose-Induced Injury in Human Umbilical Vein Endothelial Cells through the PI3K/Akt/eNOS Pathway and Regulation of Bcl-2/Bax.

J Vasc Res 2021 Jul 2:1-10. Epub 2021 Jul 2.

Department of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.

Endothelial dysfunction plays a central role in the patho-genesis of diabetic vascular complications. 2,3,5,4'-tetra-hydroxystilbene-2-O-β-D-glucoside (TSG), an active component extracted from the roots of Polygonum multiflorum Thunb, has been shown to have strong antioxidant and antiapoptotic activities. In the present study, we investigated the protective effect of TSG on apoptosis induced by high glucose in human umbilical vein endothelial cells (HUVECs) and the possible mechanisms. Read More

View Article and Full-Text PDF

Neurochemical changes underlying cognitive impairment in olfactory bulbectomized rats and the impact of the mGlu-positive allosteric modulator CDPPB.

Brain Res 2021 Jul 1;1768:147577. Epub 2021 Jul 1.

Maj Institute of Pharmacology, Polish Academy of Sciences, Department of Neurobiology, 12 Smętna Street, 31-343 Kraków, Poland. Electronic address:

The olfactory bulbectomized (OBX) rat model is a well-established model of depression in which antidepressant drugs reverse deficits in the passive avoidance test 14 days after administration. Recently, the olfactory bulbectomized rat model has been proposed to be a model of Alzheimer's disease (AD), and the available data indicate similarities between the changes that typically occur in AD and those observed in OBX animals. In the present study, the occurrence of neurochemical impairments related to AD were investigated 8 months after OB ablation. Read More

View Article and Full-Text PDF

Ferulic Acid Derivatives and Avenanthramides Modulate Endothelial Function through Maintenance of Nitric Oxide Balance in HUVEC Cells.

Nutrients 2021 Jun 12;13(6). Epub 2021 Jun 12.

Health Sciences Research Centre, Life Sciences Department, Whitelands College, University of Roehampton, London SW15 4JD, UK.

Wholegrain oats contain a variety of phenolic compounds thought to help maintain healthy vascular function, through the maintenance of local levels of the vasodilator nitric oxide (NO). Thus, the full molecular mechanisms involved are not yet clear. With this work we aim to understand the possible cellular mechanisms by which avenanthramides and ferulic acid derivatives, present in oats, may help maintain a healthy vascular function through the modulation of the NO pathway. Read More

View Article and Full-Text PDF

Extract Increases Nitric Oxide Production in Human Umbilical Vein Endothelial Cells.

Pharmaceuticals (Basel) 2021 Jun 17;14(6). Epub 2021 Jun 17.

Department of Nutrition, I-Shou University, Kaohsiung 82445, Taiwan.

The vascular nitric oxide (NO) system has a protective effect in atherosclerosis. NO is generated from the conversion of L-arginine to L-citrulline by the enzymatic action of endothelial NO synthase (eNOS). Compounds with the effect of enhancing eNOS expression are considered to be candidates for the prevention of atherosclerosis. Read More

View Article and Full-Text PDF

Activation of AMP kinase ameliorates kidney vascular dysfunction, oxidative stress and inflammation in rodent models of obesity.

Br J Pharmacol 2021 Jun 30. Epub 2021 Jun 30.

Departamento de Fisiología, Facultad de Farmacia, Universidad Complutense, Madrid, Spain.

Background And Purpose: Obesity is a risk factor for the development of chronic kidney disease independent of diabetes, hypertension and other co-morbidities. Obesity-associated nephropathy is linked to dysregulation of the cell energy sensor AMP-activated protein kinase (AMPK). We aimed here to assess whether impairment of AMPK activity may cause renal arterial dysfunction in obesity and to evaluate the therapeutic potential of activating renal AMPK. Read More

View Article and Full-Text PDF

The Inhibitory Effect of Lysophosphatidylcholine on Proangiogenesis of Human CD34 Cells Derived Endothelial Progenitor Cells.

Front Mol Biosci 2021 10;8:682367. Epub 2021 Jun 10.

Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, China.

Increasing evidence reveals that lysophosphatidylcholine (LPC) is closely related to endothelial dysfunction. The present study aimed to investigate the mechanism of LPC in inhibiting the proangiogenesis and vascular inflammation of human endothelial progenitor cells (EPCs) derived from CD34 cells. The early EPCs were derived from CD34 hematopoietic stem cells whose purity was identified using flow cytometry analysis. Read More

View Article and Full-Text PDF

Non-energy mechanism of phosphocreatine on the protection of cell survival.

Biomed Pharmacother 2021 Jun 24;141:111839. Epub 2021 Jun 24.

Department of Pharmacology, Dalian Medical University, 9 West Section, South Road of Lushun, 116044 Dalian, China. Electronic address:

If mitochondrial energy availability or oxidative metabolism is altered, patients will suffer from insufficient energy supply Phosphocreatine (PCr) not only acts as an energy carrier, but also acts as an antioxidant and defensive agent to maintain the integrity and stability of the membrane, to maintain ATP homeostasis through regulating mitochondrial respiration. Meanwhile, PCr can enhance calcium balance and reduce morphological pathological changes, ultimately, PCr helps to reduce apoptosis. On the other aspect, the activities of ATP synthase and MitCK play a crucial role in the maintenance of cellular energy metabolic function. Read More

View Article and Full-Text PDF

PM2.5 induces endothelial dysfunction via activating NLRP3 inflammasome.

Environ Toxicol 2021 Jun 26. Epub 2021 Jun 26.

Department of Cardiology, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, China.

PM2.5 (particulate matter <2.5 μm in diameter) is proven to contribute to the development of atherosclerosis. Read More

View Article and Full-Text PDF

AMPK/SIRT1 signaling through p38MAPK mediates Interleukin-6 induced neuroendocrine differentiation of LNCaP prostate cancer cells.

Biochim Biophys Acta Mol Cell Res 2021 Sep 22;1868(10):119085. Epub 2021 Jun 22.

Department of Applied Biology, CSIR-Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad 201002, India. Electronic address:

Neuroendocrine Prostate Cancer (NEPC) is an aggressive form of androgen independent prostate cancer (AIPC), correlated with therapeutic resistance. Interleukin (IL)-6 promotes proliferation and neuroendocrine differentiation (NED) of androgen dependent LNCaP cells. We treated LNCaP cells with IL-6 and observed for in vitro NED of cells and also expression of NE markers βIII tubulin, neuron-specific enolase (NSE) and chromogranin A (ChA). Read More

View Article and Full-Text PDF
September 2021

Estrogen and Preeclampsia: Potential of Estrogens as Therapeutic Agents in Preeclampsia.

Drug Des Devel Ther 2021 15;15:2543-2550. Epub 2021 Jun 15.

Reproductive Center, The First Hospital of Jilin University, Jilin University, Changchun, Jilin, 130021, People's Republic of China.

There is a significant decline in the estrogen levels in preeclampsia, and exogenous administration of estradiol normalizes blood pressure and other associated symptoms of preeclampsia. The decrease in estrogen levels may be due to changes in enzyme activities of hydroxysteroid (17-β) dehydrogenase 1, aromatase, and COMT. There is also a decrease in the novel, estrogenic G-protein-coupled receptor 30 (GPR30) in the placental trophoblast cells in preeclampsia. Read More

View Article and Full-Text PDF

Toll-like Receptor 2 (TLR2) Deficiency Abrogates Diabetic and Obese Phenotypes while Restoring Endothelial Function via Inhibition of NOX1.

Diabetes 2021 Jun 14. Epub 2021 Jun 14.

Division of Molecular Medicine, Department of Anesthesiology, Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095;

We have previously demonstrated a novel role of bone morphogenic protein-4 (BMP4) in inducing NOX1-dependent eNOS uncoupling, endothelial dysfunction, and inflammatory activation in type 2 diabetes mellitus (T2DM). However, it has remained unclear as to how BMP4 activates NOX1 and whether targeting the new mechanistic pathway revealed is effective in preserving endothelial function in T2DM. Here we observed that BMP4 induced marked, time-dependent increase in physiological binding between TLR2 and NOX1 in aortic endothelial cells, as well as increased binding of TLR2 to NOXO1. Read More

View Article and Full-Text PDF

Rosiglitazone restores nitric oxide synthase-dependent reactivity of cerebral arterioles in rats exposed to prenatal alcohol.

Alcohol Clin Exp Res 2021 Jul 12;45(7):1359-1369. Epub 2021 Jun 12.

Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD, USA.

Background: Prenatal exposure to alcohol leads to a greater incidence of many cardiovascular-related diseases, presumably via a mechanism that may involve increased oxidative stress. An agonist of peroxisome proliferator-activated receptor gamma (PPARγ; rosiglitazone) has been shown to suppress alcohol-induced neuroinflammation and oxidative stress. The goal of this study was to determine whether acute and chronic treatment with rosiglitazone could restore or prevent impaired nitric oxide synthase (NOS)-dependent responses of cerebral arterioles in male and female adult (14-16 weeks old) rats exposed to alcohol in utero. Read More

View Article and Full-Text PDF

Selective inhibition of PKCβ2 improves Caveolin-3/eNOS signaling and attenuates lipopolysaccharide-induced injury by inhibiting autophagy in H9C2 cardiomyocytes.

J Mol Histol 2021 Aug 8;52(4):705-715. Epub 2021 Jun 8.

Department of Anaesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

Lipopolysaccharide (LPS)-induced autophagy is involved in sepsis-associated myocardial injury with increased PKCβ2 activation. We previously found hyperglycemia-induced PKCβ2 activation impaired the expression of caveolin-3 (Cav-3), the dominant isoform to form cardiomyocytes caveolae which modulate eNOS signaling to confer cardioprotection in diabetes. However, little is known about the roles of PKCβ2 in autophagy and Cav-3/eNOS signaling in cardiomyocytes during LPS exposure. Read More

View Article and Full-Text PDF

Deficiency of Endothelial Nitric Oxide Synthase (eNOS) Exacerbates Brain Damage and Cognitive Deficit in A Mouse Model of Vascular Dementia.

Aging Dis 2021 Jun 1;12(3):732-746. Epub 2021 Jun 1.

1Department of Neurology, Henry Ford Hospital, Detroit, MI-48202, USA.

Vascular Dementia (VaD) accounts for nearly 20% of all cases of dementia. eNOS plays an important role in neurovascular remodeling, anti-inflammation, and cognitive functional recovery after stroke. In this study, we investigated whether eNOS regulates brain damage, cognitive function in mouse model of bilateral common carotid artery stenosis (BCAS) induced VaD. Read More

View Article and Full-Text PDF

Arginase inhibition by rhaponticin increases L-arginine concentration that contributes to Ca2+-dependent eNOS activation.

BMB Rep 2021 Jun 3. Epub 2021 Jun 3.

Department of Biological Sciences, Kangwon National University, Chuncheon 24341, Korea.

Although arginase primarily participates in the last reaction of the urea cycle, we have previously demonstrated that arginase II is an important cytosolic calcium regulator through spermine production in a p32-dependent manner. Here, we demonstrated that rhaponticin (RPT) is a novel medicinal-plant arginase inhibitor and investigated its mechanism of action on Ca2+-dependent endothelial nitric oxide synthase (eNOS) activation. RPT was uncompetitively inhibited for both arginases I and II prepared from mouse liver and kidney. Read More

View Article and Full-Text PDF

C1q/TNF-related protein-9 ameliorates hypoxia-induced pulmonary hypertension by regulating secretion of endothelin-1 and nitric oxide mediated by AMPK in rats.

Sci Rep 2021 May 31;11(1):11372. Epub 2021 May 31.

Department of Pediatrics, Xijing Hospital, Fourth Military Medical University, 127 Changlexi Road, Xi'an, 710032, China.

Injury/dysfunction of the endothelium of pulmonary arteries contributes to hypoxia-induced pulmonary hypertension (HPH). We investigated whether C1q/tumor necrosis factor-related protein-9 (CTRP9), a newly identified cardiovascular agent, has protective roles in the development of HPH. HPH was induced in adult male rats by chronic hypobaric hypoxia. Read More

View Article and Full-Text PDF

Heparan sulfate proteoglycan glypican-1 and PECAM-1 cooperate in shear-induced endothelial nitric oxide production.

Sci Rep 2021 May 31;11(1):11386. Epub 2021 May 31.

Department of Biomedical Engineering, The City College of New York, 160 Convent Ave, New York, NY, 10031, USA.

This study aimed to clarify the role of glypican-1 and PECAM-1 in shear-induced nitric oxide production in endothelial cells. Atomic force microscopy pulling was used to apply force to glypican-1 and PECAM-1 on the surface of human umbilical vein endothelial cells and nitric oxide was measured using a fluorescent reporter dye. Glypican-1 pulling for 30 min stimulated nitric oxide production while PECAM-1 pulling did not. Read More

View Article and Full-Text PDF