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Acid Sensing Ion Channels contribute to hypoxia‐induced migration in human pulmonary arterial smooth muscle cells (LB788)
Author(s) -
Yellowhair Tracylyn,
Nitta Carlos,
Herbert Lindsay,
Jernigan Nikki
Publication year - 2014
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.28.1_supplement.lb788
Subject(s) - acid sensing ion channel , hypoxia (environmental) , amiloride , cell migration , apoptosis , microbiology and biotechnology , biology , ion channel , chemistry , medicine , in vitro , biochemistry , oxygen , receptor , organic chemistry , sodium
Our laboratory has recently shown that acid sensing ion channel 1 (ASIC1) contributes to the arterial remodeling associated with chronic hypoxia‐induced pulmonary hypertension. This is consistent with the reported involvement of ASIC in migration, proliferation, and apoptosis in a variety of cells types. However, the contribution of ASIC to hypoxia‐induced migration, proliferation, and apoptosis has not been examined. Therefore, we hypothesize that ASIC1 and ASIC3 contribute to hypoxia‐induced migration in human pulmonary arterial smooth muscle cells (hPASMC). To test this hypothesis, hPASMC were grown to confluence and placed into basal media 24 hr prior to executing an in‐vitro scratch assay. Following the scratch, hPASMC were treated with a non‐selective ASIC inhibitor, amiloride; the specific ASIC1 inhibitor, psalmotoxin 1; the specific ASIC3 inhibitor, APETx2; or vehicle and then exposed to normoxia (21% oxygen, 5% CO 2 ) or hypoxia (2% oxygen, 5% CO 2 ) for 12 hrs. Inhibition of ASIC1 and ASIC3 did not alter migration of hPASMC exposed to normoxia, but prevented the hypoxia‐induced migration. This data demonstrates that ASIC1 and ASIC3 contribute to hypoxia‐induced migration in hPASMCs and describes a potential mechanism in which ASIC contributes to pulmonary arterial remodeling. We will further examine the specific role of ASIC1 and ASIC3 in hypoxia‐induced proliferation and apoptosis.