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- W948144887 abstract "Our laboratory has demonstrated an important role for acid-sensing ion channel 1 (ASIC1) in mediating increased pulmonary arterial smooth muscle cell (PASMC) Ca2+ influx and enhanced agonist-induced vasoconstriction following chronic hypoxia (CH)-induced pulmonary hypertension. ASIC1 activity is highly sensitive to changes in the redox state of the cell; in particular, hydrogen peroxide (H2O2) has been shown to inhibit ASIC1 function. Furthermore, alterations in reactive oxygen species are known to contribute to the pathogenesis of pulmonary hypertension. Therefore, we hypothesize the increased ASIC1-mediated store-operated calcium entry (SOCE) in PASMCs following CH is due to decreased H2O2, attributable to a down regulation of superoxide dismutase (SOD). We found that PEG-catalase augmented ASIC1-dependent SOCE in PASMCs from control rats, but was without effect on SOCE in PASMCs from CH rats (4 wks @ 380 Torr). However, the addition of H2O2 inhibited SOCE in both groups. Additionally, SOD1 and SOD3 protein expression were decreased in isolated pulmonary arteries from CH rats compared to control. Together these data suggest that downregulation of SOD1 and SOD3 following CH results in a loss of endogenous H2O2-induced inhibition of ASIC1-dependent SOCE in PASMC. This work is supported by NIH HL-09258 (NLJ) and HL-07736 (BRW)." @default.
- W948144887 created "2016-06-24" @default.
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- W948144887 date "2013-04-01" @default.
- W948144887 modified "2023-10-14" @default.
- W948144887 title "Loss of endogenous H 2 O 2 ‐induced inhibition of ASIC1‐mediated Ca 2+ influx in pulmonary artery smooth muscle cells following chronic hypoxia" @default.
- W948144887 doi "https://doi.org/10.1096/fasebj.27.1_supplement.1140.4" @default.
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