Abstract:
:Chemerin is an adipokine associated with increased blood pressure, and may link obesity with hypertension. We tested the hypothesis that chemerin-induced contraction of the vasculature occurs via calcium flux in smooth muscle cells. Isometric contraction of rat aortic rings was performed in parallel with calcium kinetics of rat aortic smooth muscle cells to assess the possible signaling pathway. Chemerin-9 (nonapeptide of the chemerin S157 isoform) caused a concentration-dependent contraction of isolated aorta (EC50 100nM) and elicited a concentration-dependent intracellular calcium response (EC50 10nM). Pertussis toxin (Gi inhibitor), verapamil (L-type Ca2+ channel inhibitor), PP1 (Src inhibitor), and Y27632 (Rho kinase inhibitor) reduced both calcium influx and isometric contraction to chemerin-9 but PD098059 (Erk MAPK inhibitor) and U73122 (PLC inhibitor) had little to no effect on either measure of chemerin signaling. Although our primary aim was to examine chemerin signaling, we also highlight differences in the mechanisms of chemerin-9 and recombinant chemerin S157. These data support a chemerin-induced contractile mechanism in vascular smooth muscle that functions through Gi proteins to activate L-type Ca2+ channels, Src, and Rho kinase. There is mounting evidence linking chemerin to hypertension and this mechanism brings us closer to targeting chemerin as a form of therapy.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Ferland DJ,Darios ES,Neubig RR,Sjögren B,Truong N,Torres R,Dexheimer TS,Thompson JM,Watts SWdoi
10.1016/j.vph.2016.11.009subject
Has Abstractpub_date
2017-01-01 00:00:00pages
30-41eissn
1537-1891issn
1879-3649pii
S1537-1891(16)30214-2journal_volume
88pub_type
杂志文章abstract::To investigate mechanisms of protective effects of fenofibrate on the diabetic kidney, male Wistar rats were divided into control, untreated diabetes, and fenofibrate-treated (32 mg kg(-1) d(-1), 8 weeks) diabetes groups. Diabetes induced by streptozotocin (25 mg/kg) and a high-fat diet was characterized by the disord...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.01.004
更新日期:2006-05-01 00:00:00
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journal_title:Vascular pharmacology
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doi:10.1016/j.vph.2006.10.002
更新日期:2007-03-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/j.vph.2015.02.001
更新日期:2015-04-01 00:00:00
abstract::Stem cells possess the ability of self-renewal and give rise to specific cell types. The differentiation of stem cells involves environmental factors, transduction of extra and intra-cellular signals, regulation of gene expression by transcriptional factors, microRNAs and chromosome structural modifiers. Vascular SMCs...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
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abstract::Cardiovascular diseases are the major challenge to modern medicine. Intervention to cardiovascular cells is crucial for treatment of the diseases. Here we report a novel intervention to vascular smooth muscle (VSM) cells by optogenetics. Channelrhodopsin in a tandem with YFP was selectively expressed in smooth muscle ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.03.006
更新日期:2015-08-01 00:00:00
abstract:INTRODUCTION:Growth factor therapy provides a therapeutic alternative for "no option" patients with coronary disease. Fibroblast Growth Factor-2 (FGF-2) predominantly stimulates angiogenesis, the growth of new capillaries, whereas Monocyte Chemoattractant Protein-1 (MCP-1) is considered an arteriogenic agent. We hypoth...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.01.002
更新日期:2006-05-01 00:00:00
abstract:BACKGROUND AND AIM:The aim of this study was to investigate the effect of acute hypercapnia due to the mechanical hypoventilation on the oxidative metabolism of peripheral blood neutrophils in the rabbit. METHODS:The study was performed on 24 Chinchilla rabbits, randomized into normo- and hypercapnia groups (P(a)CO(2)...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/s1537-1891(02)00338-5
更新日期:2003-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.12.004
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2009.07.001
更新日期:2009-10-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2018.02.005
更新日期:2018-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.08.001
更新日期:2010-11-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2011.06.005
更新日期:2011-11-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.11.006
更新日期:2006-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.01.009
更新日期:2008-04-01 00:00:00
abstract:BACKGROUND:Altered endothelial cell (EC)-derived mediator levels, including increased endothelin-1 (ET-1), are hallmarks of human pulmonary arterial hypertension (PAH). Gene mutations for receptors for bone morphogenic proteins (BMP), or transforming growth factor-beta (TGF-beta) cause heritable PAH. The effects of BMP...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.09.001
更新日期:2009-01-01 00:00:00
abstract::Sixty-seven male patients with hypercholesterolemia, divided into three groups according to apolipoprotein E phenotype (33 with apoE3/ 3 phenotype, E3 group; 23 with 2/2 or 2/3, E2+ group; 11 with 4/4 or 4/3, E4+ group), received daily 20-40 mg of fluvastatin for 12 weeks. The levels of triglyceride (TG), cholesterol ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2003.09.002
更新日期:2003-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.02.012
更新日期:2005-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.01.003
更新日期:2005-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.08.007
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.04.006
更新日期:2016-07-01 00:00:00
abstract::Endothelin (ET-1) is chronically elevated in diabetes. However, role of ET-1 in increased oxidative stress in type 2 diabetes is less clear. This study tested the hypotheses that: 1) oxidative stress markers are increased and total antioxidant capacity is decreased in diabetes, and 2) activation of ET(A) receptors med...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2007.05.006
更新日期:2007-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.03.002
更新日期:2005-06-01 00:00:00
abstract::The endothelium synthesizes and releases nitric oxide (NO) to maintain homeostatic function. Under basal conditions, endothelium-derived NO maintains a nonthrombogenic surface, prohibits leukocyte attachment, and promotes vascular relaxation. In the setting of clinical syndromes associated with the development of athe...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/s1537-1891(02)00250-1
更新日期:2002-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2016.05.016
更新日期:2016-11-01 00:00:00
abstract::Elevated plasma levels of factor VII and fibrinogen are risk factors for cardiovascular disease, especially arterial thrombosis. Oral contraceptive use increases factor VII and fibrinogen plasma levels. It has been described that DNA polymorphisms are associated with the plasma levels of hemostatic variables and their...
journal_title:Vascular pharmacology
pub_type: 临床试验,杂志文章,随机对照试验
doi:10.1016/s1537-1891(02)00300-2
更新日期:2002-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.01.008
更新日期:2012-03-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.09.006
更新日期:2006-01-01 00:00:00
abstract::tert-Butyl hydroperoxide (t-BOOH), a membrane permeant oxidant, elicits enhanced vasoconstriction of perfused kidney and mesenteric arterial beds isolated from DOCA-salt-induced hypertensive rats. We hypothesize that enhanced vasoconstriction to t-BOOH during DOCA-salt hypertension involves free radical species and de...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/s1537-1891(02)00309-9
更新日期:2003-01-01 00:00:00
abstract:BACKGROUND:Platelets play crucial roles in the development of arterial thrombosis and other pathophysiologies leading to clinical ischemic events. Defective regulation of platelet activation/aggregation is a predominant cause for arterial thrombosis. The purposes of the study are to determine whether atherosclerotic pl...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.03.004
更新日期:2008-07-01 00:00:00