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学科主题基础医学
Ca(v)3.1 (alpha(1G)) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells
Zhou, Chun; Chen, Hairu; Lu, Fengmin; Sellak, Hassan; Daigle, Jonathan A.; Alexeyev, Mikhail F.; Xi, Yaguang; Ju, Jingfang; van Mourik, Jan A.; Wu, Songwei
关键词endothelial cells thrombin
刊名AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
2007-04-01
DOI10.1152/ajplung.00377.2006
292期:4页:L833-L844
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Physiology ; Respiratory System
研究领域[WOS]Physiology ; Respiratory System
关键词[WOS]WEIBEL-PALADE BODIES ; GRANULE MEMBRANE-PROTEIN ; VONWILLEBRAND-FACTOR RELEASE ; T-TYPE ; P-SELECTIN ; CYTOSOLIC CA2+ ; STIMULATED SECRETION ; ADENYLYL-CYCLASE ; CALCIUM-CHANNEL ; EXOCYTOSIS
英文摘要

The T-type Ca2+ channel Ca(v)3.1 subunit is present in pulmonary microvascular endothelial cells (PMVECs), but not in pulmonary artery endothelial cells (PAECs). The present study sought to assess the role of Cav3.1 in thrombin-induced Weibel-Palade body exocytosis and consequent von Willebrand factor (VWF) release. In PMVECs and PAECs transduced with a green fluorescent protein (GFP)-tagged VWF chimera, we examined the real-time dynamics and secretory process of VWF-GFP-containing vesicles in response to thrombin and the cAMP-elevating agent isoproterenol. Whereas thrombin stimulated a progressive decrease in the number of VWF-GFP-containing vesicles in both cell types, isoproterenol only decreased the number of VWF-GFP-containing vesicles in PAECs. In PMVECs, thrombin-induced decrease in the number of VWF-GFP-containing vesicles was nearly abolished by the T-type Ca2+ channel blocker mibefradil as well as by Ca(v)3.1 gene silencing with small hairpin RNA. Expression of recombinant Ca(v)3.1 subunit in PAECs resulted in pronounced increase in thrombin-stimulated Ca2+ entry, which is sensitive to mibefradil. Together, these data indicate that VWF secretion from lung endothelial cells is regulated by two distinct pathways involving Ca2+ or cAMP, and support the hypothesis that activation of Ca(v)3.1 T-type Ca2+ channels in PMVECs provides a unique cytosolic Ca2+ source important for Gq-linked agonist-induced VWF release.

语种英语
WOS记录号WOS:000247935500003
引用统计
被引频次:18[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/68129
专题北京大学基础医学院_病原生物学系
作者单位1.Univ S Alabama, Coll Med, Ctr Lung Biol, Mobile, AL 36688 USA
2.Univ S Alabama, Coll Med, Dept Pharmacol, Mobile, AL 36688 USA
3.Univ S Alabama, Coll Med, Dept Physiol, Mobile, AL 36688 USA
4.Univ S Alabama, Coll Med, Dept Cell Biol, Mobile, AL 36688 USA
5.Univ S Alabama, Coll Med, Dept Neurosci, Mobile, AL 36688 USA
6.Peking Univ, Hlth Sci Ctr, Dept Microbiol, Beijing 100871, Peoples R China
7.Univ S Alabama, Mitchell Canc Inst, Canc Genom Lab, Mobile, AL 36688 USA
8.Sanquin Res, Dept Plasma Prot, Amsterdam, Netherlands
9.Landsteiner Lab, Amsterdam, Netherlands
10.Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1105 AZ Amsterdam, Netherlands
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Zhou, Chun,Chen, Hairu,Lu, Fengmin,et al. Ca(v)3.1 (alpha(1G)) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells[J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,2007,292(4):L833-L844.
APA Zhou, Chun.,Chen, Hairu.,Lu, Fengmin.,Sellak, Hassan.,Daigle, Jonathan A..,...&Wu, Songwei.(2007).Ca(v)3.1 (alpha(1G)) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells.AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,292(4),L833-L844.
MLA Zhou, Chun,et al."Ca(v)3.1 (alpha(1G)) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells".AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 292.4(2007):L833-L844.
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