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Alteration of CD38 and Two‐Pore Channels expression by hypoxia exposure in Pulmonary Arterial Smooth Muscle
Author(s) -
Lee Suengwon,
Jiang Yongliang,
Sham James S.K.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.871.4
Subject(s) - cd38 , hypoxia (environmental) , ryanodine receptor , endoplasmic reticulum , glomus cell , biology , chemistry , microbiology and biotechnology , biochemistry , medicine , endocrinology , receptor , oxygen , chemoreceptor , stem cell , organic chemistry , cd34
CD38 is a multifunctional enzyme responsible for the synthesis of cyclic adenosine diphosphated‐ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP). cADPR and NAADP trigger Ca2+ release via ryanodine receptors of sarcoplasmic reticulum and NAADP‐sensitive two‐pore channels (TPCs) of lysosomal stores, respectively, and are thought to play important roles in regulation of [Ca2+]i and vascular functions. We recently examined the expression of CD38 and TPC1/2 in various rat arterial smooth muscles. Pulmonary artery (PA) has higher expression of CD38 and TPC1/2 compared to other systemic arteries. However, there is little information on the changes in expression and function of CD38 and TPCs in PA under hypoxia. Here, we used western blot analysis and quantitative real‐time PCR to examine the alteration of expression of CD38 and TPC1/2 in PA smooth muscle cells. Rats were exposed to hypoxic condition (10% O2) up to 1 week in hypoxic chamber. Endothelium‐removed PA tissues were collected in day 0, 1, 2, 3 and 7. Both CD38 protein and mRNA were significantly increased during hypoxia compared to day 0. Likewise, TPC1/2 proteins were significantly elevated after hypoxic exposure. Our results show that expression of CD38 and TPC1/2 in PA are upregulated by prolonged hypoxia; the elevation of their expression may contribute to the alterations in Ca2+ homeostasis in hypoxic pulmonary hypertension.