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学科主题: 基础医学
题名:
Ca(v)3.1 (alpha(1G)) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells
作者: 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
发表日期: 2007-04-01
DOI: 10.1152/ajplung.00377.2006
卷: 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
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/68129
Appears in Collections:基础医学院_病原生物学系_期刊论文

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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

Recommended Citation:
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.
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