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Hypoxia inducible factor-1-dependent up-regulation of BMP4 mediates hypoxia-induced increase of TRPC expression in PASMCs
Author(s) -
Jian Wang,
Xin Fu,
Kai Yang,
Jiang Qian,
Yuqin Chen,
Jing Jia,
Xin Duan,
Elizabeth W. Wang,
Jianxing He,
Pixin Ran,
Nanshan Zhong,
Gregg L. Semenza,
Wenju Lu
Publication year - 2015
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvv122
Subject(s) - trpc , gene knockdown , bone morphogenetic protein 4 , hypoxia (environmental) , endocrinology , noggin , medicine , biology , downregulation and upregulation , microbiology and biotechnology , chemistry , transient receptor potential channel , receptor , bone morphogenetic protein , gene , biochemistry , organic chemistry , oxygen
Previously we demonstrated that both hypoxia inducible factor-1 (HIF-1) and bone morphogenetic protein-4 (BMP4) up-regulate transient receptor potential canonical (TRPC) 1 and TRPC6, resulting in increased basal intracellular Ca(2+) concentration ([Ca(2+)]i) in pulmonary arterial smooth muscle cells (PASMCs), driving development of chronic hypoxia (CH)-induced pulmonary hypertension (CHPH). This study aims to determine whether HIF-1 regulates BMP4, and whether BMP4 mediates TRPC and basal [Ca(2+)]i increases in hypoxic PASMCs.

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