Role of Cl− currents in rat aortic smooth muscle activation by prostaglandin F2α

2003 ◽  
Vol 481 (2-3) ◽  
pp. 133-140 ◽  
Author(s):  
Jihua Jiang ◽  
Peter H Backx ◽  
Hwee Teoh ◽  
Michael E Ward
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
Prostaglandin F2α ◽  
Aortic Smooth Muscle

scholarly journals The Role of Two-Pore Channels in Norepinephrine-Induced [Ca2+]i Rise in Rat Aortic Smooth Muscle Cells and Aorta Contraction

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1144 ◽  
Author(s):  
Sergei K. Trufanov ◽  
Elena Yu. Rybakova ◽  
Piotr P. Avdonin ◽  
Alexandra A. Tsitrina ◽  
Irina L. Zharkikh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Calcium Concentration ◽  
Muscle Cells ◽  
Rat Aorta ◽  
Structural Analogue ◽  
Aortic Smooth Muscle ◽  
Cis And Trans ◽  
High Degree

Second messenger nicotinic acid adenine dinucleotide phosphate (NAADP) triggers Ca2+ release via two-pore channels (TPCs) localized in endolysosomal vesicles. The aim of the present work is to evaluate the role of TPCs in the action of norepinephrine (NE), angiotensin II (AngII), vasopressin (AVP), and 5-hydroxytriptamine (5-HT) on free cytoplasmic calcium concentration ([Ca2+]i) in smooth muscle cells (SMCs) isolated from rat aorta and on aorta contraction. To address this issue, the NAADP structural analogue and inhibitor of TPCs, NED 19, was applied. We have demonstrated a high degree of colocalization of the fluorescent signals of cis-NED 19 and endolysosmal probe LysoTracker in SMCs. Both cis- or trans-NED 19 inhibited the rise of [Ca2+]i in SMCs induced by 100 μM NE by 50–60%. IC50 for cis- and trans-NED 19 were 2.7 and 8.9 μM, respectively. The inhibition by NED 19 stereoisomers of the effects of AngII, AVP, and 5-HT was much weaker. Both forms of NED 19 caused relaxation of aortic rings preconstricted by NE, with relative potency of cis-NED 19 several times higher than that of trans-NED 19. Inhibition by cis-NED 19 of NE-induced contraction was maintained after intensive washing and slowly reversed within an hour of incubation. Cis- and trans-NED 19 did not cause decrease in the force of aorta contraction in response to Ang II and AVP, and only slightly relaxed aorta preconstricted by 5-HT and by KCl. Suppression of TPC1 in SMCs with siRNA caused a 40% decrease in [Ca2+]i in response to NE, whereas siRNA against TPC2 did not change NE calcium signaling. These data suggest that TPC1 is involved in the NE-stimulated [Ca2+]i rise in SMCs. Inhibition of TPC1 activity by NED 19 could be the reason for partial inhibition of aortic rings contraction in response to NE.

Novel role for K+-dependent Na+/Ca2+ exchangers in regulation of cytoplasmic free Ca2+ and contractility in arterial smooth muscle

2006 ◽  
Vol 291 (3) ◽  
pp. H1226-H1235 ◽  
Author(s):  
Hui Dong ◽  
Yanfen Jiang ◽  
Chris R. Triggle ◽  
Xiaofang Li ◽  
Jonathan Lytton
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Tone ◽  
Rt Pcr ◽  
Aortic Smooth Muscle ◽  
Voltage Gated ◽  
Reverse Mode ◽  
And Function ◽  
Contraction And Relaxation

Cytoplasmic free Ca2+ ([Ca2+]cyt) is essential for the contraction and relaxation of blood vessels. The role of plasma membrane Na+/Ca2+ exchange (NCX) activity in the regulation of vascular Ca2+ homeostasis was previously ascribed to the NCX1 protein. However, recent studies suggest that a relatively newly discovered K+-dependent Na+/Ca2+ exchanger, NCKX (gene family SLC24), is also present in vascular smooth muscle. The purpose of the present study was to identify the expression and function of NCKX in arteries. mRNA encoding NCKX3 and NCKX4 was demonstrated by RT-PCR and Northern blot in both rat mesenteric and aortic smooth muscle. NCXK3 and NCKX4 proteins were also demonstrated by immunoblot and immunofluorescence. After voltage-gated Ca2+ channels, store-operated Ca2+ channels, and Na+ pump were pharmacologically blocked, when the extracellular Na+ was replaced with Li+ (0 Na+) to induce reverse mode (Ca2+ entry) activity of Na+/Ca2+ exchangers, a large increase in [Ca2+]cyt signal was observed in primary cultured aortic smooth muscle cells. About one-half of this [Ca2+]cyt signal depended on the extracellular K+. In addition, after the activity of NCX was inhibited by KB-R7943, Na+ replacement-induced Ca2+ entry was absolutely dependent on extracellular K+. In arterial rings denuded of endothelium, a significant fraction of the phenylephrine-induced and nifedipine-resistant aortic or mesenteric contraction could be prevented by removal of extracellular K+. Taken together, these data provide strong evidence for the expression of NCKX proteins in the vascular smooth muscle and their novel role in mediating agonist-stimulated [Ca2+]cyt and thereby vascular tone.

scholarly journals The role of cytoskeleton in the regulation of contractile activity in smooth muscle cells from aorta of rats

2007 ◽  
Vol 6 (1) ◽  
pp. 78-82
Author(s):  
S. V. Gousakova
Keyword(s):  
Smooth Muscle ◽  
Contractile Activity ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Aortic Smooth Muscle ◽  
Physiologically Active Substances ◽  
Cytochalasine B ◽  
Smooth Muscle Contractions ◽  
System Operating

Influence of cytoskeleton modulation by Colchicine and Cytochalasine B on contractile reactions of smooth muscle segments of rat's aorta caused by physiologically active substances, the membrane's depolarization and cells' striction was investigated by mechanographical method. Microtubules and actinic elements of the cytoskeleton were established to participate in the development of hyper-potassic and phenylephrine -induced contractions as well as in the smooth muscle relaxation induced by cAMP. Cytochalasine B suppresses both kinds of aortic smooth muscle contractions more effectively than Colchicine. Contractile reactions at isoosmotic striction are suppressed only by Cytochalasine. Efficacy of cAMP signal system operating depends on actinic cyto-skeleton integrity.

scholarly journals LncRNA SCIRT is downregulated in atherosclerosis and suppresses the proliferation of human aortic smooth muscle cells (HAOSMCs) by sponging miR-146a in cytoplasm

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Wenhui Gao ◽  
Rong Li ◽  
Jingjing Yu ◽  
Xijie He ◽  
Duo Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cancer Biology ◽  
Direct Interaction ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Brdu Assay

Abstract Background SCIRT has been characterized as a key player in cancer biology, while its role in other human diseases is unclear. This study explored its role in atherosclerosis, with a specific focus on its interaction with SCIRT and miR-146a. Methods The expression of SCIRT and miR-146a in atherosclerosis-affected tissues and healthy tissues from 56 atherosclerosis patients were analyzed by RT-qPCR. The expression of SCIRT in nuclear and cytoplasm samples was detected by RNA fractionation assay. The direct interaction between SCIRT and miR-146a was detected by RNA pull-down assay. SCIRT and miR-146a were overexpressed in human aortic smooth muscle cells (HAOSMCs) to study the crosstalk between them. The role of SCIRT and miR-146a in the proliferation of HAOSMCs was analyzed with BrdU assay. Results SCIRT was downregulated by atherosclerosis, while miR-146a was upregulated by atherosclerosis. SCIRT was detected in both cytoplasm and nuclear samples, and it directly interacted with miR-146a. In HAOSMCs, overexpression of SCIRT and miR-146a did not affect the expression of each other. Interestingly, SCIRT suppressed the proliferation of HAOSMCs and reduced the enhancing effects of miR-146a on cell proliferation. Conclusion Therefore, SCIRT is downregulated in atherosclerosis and it suppresses the proliferation of HAOSMCs by sponging miR-146a in cytoplasm.

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