کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5513171 | 1540979 | 2017 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Testosterone rapidly increases Ca2+-activated K+ currents causing hyperpolarization in human coronary artery endothelial cells
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
EGTADIDSU-73122KCaPLCpKaPTXH-89eNOSKirNOSHCAECNSCGi/o proteinHEPESSKCaTrphyperpolarizationlarge conductance Ca2+-activated K+ channelNω-nitro-L-arginine methylesterFBSDHTKATP4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid - 4- (2-hydroxyethyl) -1-piperazineethanesulfonic acid4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid - 4،4'-diisothiocyanatostilbene-2،2'-disulfonic acidBKCa - BKC بهDMSO - DMSOIKCa - IKC بهl-NAME - L-NAMEAndrogen - آندروژنethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid - اتیلن گلیکول بیس (β-آمینویل اتر) -N، N، N '، N'-tetraacetic اسیدepoxyeicosatrienoic acid - اسید اپوکسی اسیاتریتروئینTetraethylammonium - تترا اتیل آمونیومanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancestandard error of the mean - خطای استاندارد میانگینEET - خوردنDihydrotestosterone - دی هیدروتستوسترونDimethyl sulfoxide - دیمتیل سولفواکسیدfetal bovine serum - سرم جنین گاوHuman coronary artery endothelial cell - سلول اندوتلیال عروق کرونر انسانیpertussis toxin - سموم سورافنیphospholipase C - فسفولیپاز CSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازprotein kinase A - پروتئین کیناز ATEA - چایATP-sensitive K+ channel - کانال K + حساس به ATPCa2+-activated K+ channel - کانال K + فعال شده Ca2 +inward rectifier K+ channel - کانال K + یکسو کننده داخلیTransient receptor potential channel - کانال بالقوه گیرنده گذراNonselective cation channel - کانال غیر کیهانی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Testosterone has endothelium-dependent vasodilatory effects on the coronary artery, with some reports suggesting endothelial ion channel involvement. This study employed the whole-cell patch clamp technique to investigate the effect of testosterone on ion channels in human coronary artery endothelial cells (HCAECs) and the mechanisms involved. We found that 0.03-3 μM testosterone significantly induced a rapid, concentration-dependent increase in total HCAEC current (EC50, 71.96 ± 1.66 nM; maximum increase, 59.13 ± 8.37%; mean ± SEM). The testosterone-enhanced currents consisted of small- and large-conductance Ca2+-activated K+ currents (SKCa and BKCa currents), but not Clâ and nonselective cation currents. Either a non-permeant testosterone conjugate or the non-aromatizable androgen dihydrotestosterone (DHT) could increase HCAEC currents as well. The androgen receptor antagonist flutamide prevented this testosterone, testosterone conjugate, and DHT effect, while the estrogen receptor antagonist fulvestrant did not. Incubating HCAECs with pertussis toxin or protein kinase A inhibitor H-89 largely inhibited the testosterone effect, while pre-incubation with phospholipase C inhibitor U-73122, prostacyclin inhibitor indomethacin, nitric oxide synthase inhibitor L-NAME or cytochrome P450 inhibitor MS-PPOH, did not. Finally, testosterone application induced HCAEC hyperpolarization within minutes; this effect was prevented by SKCa and BKCa current inhibitors apamin and iberiotoxin. This is the first electrophysiological demonstration of androgen-induced KCa current increase, leading to hyperpolarization, in any endothelial cell, and the first report of SKCa as a testosterone target. Our data show that testosterone rapidly increased whole-cell HCAEC SKCa and BKCa currents via a surface androgen receptor, Gi/o protein, and protein kinase A. This mechanism may explain rapid testosterone-induced coronary vasodilation seen in vivo.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 168, April 2017, Pages 118-126
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 168, April 2017, Pages 118-126
نویسندگان
Katesirin Ruamyod, Wattana B. Watanapa, Chairat Shayakul,