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Search results for: Endothelin

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#35043652   2022/01/19 To Up

Combined effect of acute altitude exposure and vigorous exercise on platelet activation.

Exposure to high altitudes and exercise alters body's physiology and may cause acute cardiovascular events. Platelet activation is one of the key players in these events. Therefore, we investigated the effect of vigorous exercise at higher altitude (2650 m) on platelet aggregation and serum markers of platelet activation. 14 healthy subjects performed a step incremental ergometer test until exhaustion at the Environmental Research Station (UFS, 2650 m) at Zugspitze. Platelet aggregation and serum levels of endothelin-1, soluble p-selectin, platelet factor 4 and Chromogranin A were measured. Platelet activation was significantly enhanced after exercise at high altitude compared to measures immediately prior exercise. We detected significantly enhanced serum levels of endothelin-1 and soluble p-selectin whereas chromogranin A and platelet factor 4 remained unchanged. This effect might be due to increased endothelin-1 levels causing pulmonary vasoconstriction, rheological changes and direct platelet activation. This might be of clinical relevance, especially in patients with pre-existing diseases.
K Lackermair, D Schüttler, A Kellnar, C G Schuhmann, L T Weckbach, S Brunner

1512 related Products with: Combined effect of acute altitude exposure and vigorous exercise on platelet activation.

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#35043642   2022/01/19 To Up

Association of polymorphisms in endothelin-1 and endothelin receptor a genes with vasovagal syncope.

The endothelin system may play a role in the pathogenesis of vasovagal syncope (VVS) because it is implicated in blood pressure regulation. We hypothesized that endothelin-related genetic polymorphisms might modulate susceptibility to VVS. This study aimed to evaluate the possible influence of endothelin-1 (EDN1) and endothelin receptor A (EDNRA) gene variants on the occurrence of tilt-induced VVS and autonomic nervous system activity during the head-up tilt test (HUT). Results were expressed as mean +/- SEM. In 254 patients with recurrent syncope (age 45.33+/-1.22 years, 94 males, 160 females), heart rate variability (HRV) was measured during HUT. EDN1 rs5370 G>T and EDNRA rs5333 T>C gene polymorphisms were assessed using high-resolution melting analysis. There was no statistically significant association between polymorphisms EDN1 rs5370 and EDNRA rs5333 and positivity of HUT or hemodynamic types of VVS. Patients with GT or TT genotypes at the rs5370 locus of the EDN1 had significantly higher values of high-frequency (HF) and the standard deviation of the average NN intervals at the time of the syncope, and they tended to have lower low-frequency (LF) and LF/HF ratio when compared to homozygotes (GG). No statistically significant differences were found in HRV parameters concerning the EDNRA rs5333 genotypes. Our findings suggest the potential role of EDN1 rs5370 variants in regulating autonomic nervous activity and pathogenesis of VVS.
Z Lazurova, V Habalova, P Mitro

1407 related Products with: Association of polymorphisms in endothelin-1 and endothelin receptor a genes with vasovagal syncope.

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#35036886   2021/11/25 To Up

Vasoconstrictor antagonism improves functional and structural vascular alterations and liver damage in rats with early NAFLD.

Intrahepatic vascular resistance is increased in early non-alcoholic fatty liver disease (NAFLD), potentially leading to tissue hypoxia and triggering disease progression. Hepatic vascular hyperreactivity to vasoconstrictors has been identified as an underlying mechanism. This study investigates vasoconstrictive agonism and antagonism in 2 models of early NAFLD and in non-alcoholic steatohepatitis (NASH).
Denise van der Graaff, Shivani Chotkoe, Benedicte De Winter, Joris De Man, Christophe Casteleyn, Jean-Pierre Timmermans, Isabel Pintelon, Luisa Vonghia, Wilhelmus J Kwanten, Sven Francque

2422 related Products with: Vasoconstrictor antagonism improves functional and structural vascular alterations and liver damage in rats with early NAFLD.

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#35032586   2022/01/12 To Up

Classical prescription Dachuanxiong Formula delays nitroglycerin-induced pain response in migraine mice through reducing endothelin-1 level and regulating fatty acid biosynthesis.

Dachuanxiong Formula (DCXF) is a classical Chinese medicine prescription and is composed of dried rhizomes from Ligusticum striatum DC. (Chuanxiong Rhizoma) and Gastrodia elata Bl. (Gastrodiae Rhizoma) at the ratio of 4:1 (w/w). It has been used as Chinese medicine prescription for thousands of years. DCXF is used traditionally to treat many diseases, including migraine, atherosclerosis and ischemic stroke.
Chi Teng Vong, Yulong Chen, Zhejie Chen, Caifang Gao, Fengqing Yang, Shengpeng Wang, Yitao Wang

1063 related Products with: Classical prescription Dachuanxiong Formula delays nitroglycerin-induced pain response in migraine mice through reducing endothelin-1 level and regulating fatty acid biosynthesis.

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#35026265   2022/01/10 To Up

Identification of the hormetic dose-response and regulatory network of multiple metals co-exposure-related hypertension via integration of metallomics and adverse outcome pathways.

Environmental stressors, including heavy metals, can be associated with hypertension development. However, little information regarding the dose-response relationship and toxicity mechanisms of metal mixtures with hypertension development is currently available. Therefore, we recruited 940 participants from six factories in northeastern China and measured the urinary concentrations of 19 metals. Then, we used Bayesian kernel machine regression (BKMR) to explore associations between metals co-exposure and hypertension. The BKMR model indicated a hermetic dose-response relationship between eight urinary metals (Co, Cr, Ni, Cd, As, Fe, Zn, and Pb) and hypertension risk. Moreover, heterogeneous and non-linear association patterns were detected across different metals/metalloids concentrations. Next, for the first time, we analyzed data of chemicals containing specific metal elements in the Comparative Toxicogenomics Database (CTD) from a disease perspective and provided insights from various biological levels to explain heavy metal co-exposure-related hypertension. On the molecular scale, 43 chemical components and 112 potential target genes were detected for metal exposure-related hypertension. Further, the network topology analysis indicated that target genes such as insulin (INS, degree = 78), albumin (ALB, degree = 74), renin (REN, degree = 71), interleukin-6 (IL6, degree = 70), endothelin 1 (EDN1, degree = 70), and endothelial nitric oxide synthase (NOS3, degree = 69) have a strong correlation with heavy metals co-exposure. Finally, we used integrative analyses in the adverse outcome pathway (AOP) wiki to analyze the co-exposure of heavy metals and hypertension and support an integrated metallomics approach. We selected the AOP 149 as the framework and found that the molecular initiating events (MIEs) of hypertension stems from the oxidation of AA residues on critical peptides of the NO pathway. The NOS3 was particularly promising since its subunit has three metal ion cross-linking domains with Zn, Fe, and Ga, which might serve as a binding site for heavy metal ions.
Peng Shi, Shengnan Liu, Xinyu Xia, Jili Qian, Hongmei Jing, Jiamei Yuan, Hanqing Zhao, Fei Wang, Yue Wang, Xue Wang, Xuan Wang, Miao He, Shuhua Xi

1077 related Products with: Identification of the hormetic dose-response and regulatory network of multiple metals co-exposure-related hypertension via integration of metallomics and adverse outcome pathways.

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#35017014   2022/01/10 To Up

G3bp1 - microRNA-1 axis regulates cardiomyocyte hypertrophy.

Adaptation of gene expression is one of the most fundamental response of cardiomyocytes to hypertrophic stimuli. G3bp1, an RNA binding protein with site-specific endoribonuclease activity regulates the processing of pre-miR-1 stem-loop, and thus levels of cardiomyocyte -enriched mature miR-1. Here, we examine the role of G3bp1 in regulating gene expression in quiescent cardiomyocytes and those undergoing growth-factor induced hypertrophy. Further, we determine if these changes are facilitated through G3bp1-mediated regulation of miR-1 in these cardiomyocytes. Using isolated cardiomyocytes with knockdown of endogenous G3bp1, we performed high throughput RNA sequencing to determine the change in cardiac transcriptome. Then, using gain and loss of function approach for both, G3bp1 and miR-1, alone or in combination we examine the G3bp1-miR-1 signaling in regulating gene expression and Endothelin (ET-1) -induced cardiomyocyte hypertrophy. We show that knockdown of endogenous G3bp1 results in inhibition of genes involved in calcium handling, cardiac muscle contraction, action potential and sarcomeric structure. In addition, there is inhibition of genes that contribute to hypertrophic and dilated cardiomyopathy development. Conversely, an increase is seen in genes that negatively regulate the Hippo signaling, like Rassf1 and Arrdc3, along with inflammatory genes of TGF-β and TNF pathways. Knockdown of G3bp1 restricts ET-1 induced cardiomyocyte hypertrophy. Interestingly, concurrent silencing of G3bp1 and miR-1 rescues the change in gene expression and inhibition of hypertrophy seen with knockdown of G3bp1 alone. Similarly, expression of exogenous G3bp1 reverses the miR-1 induced inhibition of gene expression. Intriguingly, expression of Gfp tagged G3bp1 results in perinuclear accumulations of G3bp1-Gfp, resembling Stress Granules. Based on our results, we conclude that G3bp1 through its regulation of mature miR-1 levels plays a critical role in regulating the expression of essential cardiac-enriched genes and those involved in development of cardiomyocyte hypertrophy.
Saleena Alikunju, Nandita Niranjan, Maha Mohsin, Nazish Sayed, Danish Sayed

2611 related Products with: G3bp1 - microRNA-1 axis regulates cardiomyocyte hypertrophy.

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#35013491   2022/01/10 To Up

Endothelial-derived extracellular microRNA-92a promotes arterial stiffness by regulating phenotype changes of vascular smooth muscle cells.

Endothelial dysfunction and vascular smooth muscle cell (VSMC) plasticity are critically involved in the pathogenesis of hypertension and arterial stiffness. MicroRNAs can mediate the cellular communication between vascular endothelial cells (ECs) and neighboring cells. Here, we investigated the role of endothelial-derived extracellular microRNA-92a (miR-92a) in promoting arterial stiffness by regulating EC-VSMC communication. Serum miR-92a level was higher in hypertensive patients than controls. Circulating miR-92a level was positively correlated with pulse wave velocity (PWV), systolic blood pressure (SBP), diastolic blood pressure (DBP), and serum endothelin-1 (ET-1) level, but inversely with serum nitric oxide (NO) level. In vitro, angiotensin II (Ang II)-increased miR-92a level in ECs mediated a contractile-to-synthetic phenotype change of co-cultured VSMCs. In Ang II-infused mice, locked nucleic acid-modified antisense miR-92a (LNA-miR-92a) ameliorated PWV, SBP, DBP, and impaired vasodilation induced by Ang II. LNA-miR-92a administration also reversed the increased levels of proliferative genes and decreased levels of contractile genes induced by Ang II in mouse aortas. Circulating serum miR-92a level and PWV were correlated in these mice. These findings indicate that EC miR-92a may be transported to VSMCs via extracellular vesicles to regulate phenotype changes of VSMCs, leading to arterial stiffness.
Chen Wang, Haoyu Wu, Yuanming Xing, Yulan Ye, Fangzhou He, Qian Yin, Yujin Li, Fenqing Shang, John Y-J Shyy, Zu-Yi Yuan

2005 related Products with: Endothelial-derived extracellular microRNA-92a promotes arterial stiffness by regulating phenotype changes of vascular smooth muscle cells.

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#35012642   2022/01/10 To Up

Thymosin beta-4 improves endothelial function and reparative potency of diabetic endothelial cells differentiated from patient induced pluripotent stem cells.

Prior studies show that signature phenotypes of diabetic human induced pluripotent stem cells derived endothelial cells (dia-hiPSC-ECs) are disrupted glycine homeostasis, increased senescence, impaired mitochondrial function and angiogenic potential as compared with healthy hiPSC-ECs. In the current study, we aimed to assess the role of thymosin β-4 (Tb-4) on endothelial function using dia-hiPSC-ECs as disease model of endothelial dysfunction.
Liping Su, Xiaocen Kong, Szejie Loo, Yu Gao, Bingli Liu, Xiaofei Su, Rinkoo Dalan, Jianhua Ma, Lei Ye

2955 related Products with: Thymosin beta-4 improves endothelial function and reparative potency of diabetic endothelial cells differentiated from patient induced pluripotent stem cells.

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#35008670   2021/12/27 To Up

Autoantibodies Targeting AT- and ET-Receptors Link Endothelial Proliferation and Coagulation via Ets-1 Transcription Factor.

Scleroderma renal crisis (SRC) is an acute life-threatening manifestation of systemic sclerosis (SSc) caused by obliterative vasculopathy and thrombotic microangiopathy. Evidence suggests a pathogenic role of immunoglobulin G (IgG) targeting G-protein coupled receptors (GPCR). We therefore dissected SRC-associated vascular obliteration and investigated the specific effects of patient-derived IgG directed against angiotensin II type 1 (ATR) and endothelin-1 type A receptors (ETR) on downstream signaling events and endothelial cell proliferation. SRC-IgG triggered endothelial cell proliferation via activation of the mitogen-activated protein kinase (MAPK) pathway and subsequent activation of the E26 transformation-specific-1 transcription factor (Ets-1). Either ATR or ETR receptor inhibitors/shRNA abrogated endothelial proliferation, confirming receptor activation and Ets-1 signaling involvement. Binding of Ets-1 to the tissue factor (TF) promoter exclusively induced TF. In addition, TF inhibition prevented endothelial cell proliferation. Thus, our data revealed a thus far unknown link between SRC-IgG-induced intracellular signaling, endothelial cell proliferation and active coagulation in the context of obliterative vasculopathy and SRC. Patients' autoantibodies and their molecular effectors represent new therapeutic targets to address severe vascular complications in SSc.
Rusan Catar, Melanie Herse-Naether, Nan Zhu, Philine Wagner, Oskar Wischnewski, Angelika Kusch, Julian Kamhieh-Milz, Andreas Eisenreich, Ursula Rauch, Björn Hegner, Harald Heidecke, Angela Kill, Gabriela Riemekasten, Gunnar Kleinau, Patrick Scheerer, Duska Dragun, Aurelie Philippe

1470 related Products with: Autoantibodies Targeting AT- and ET-Receptors Link Endothelial Proliferation and Coagulation via Ets-1 Transcription Factor.

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