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BK channels in rat and human pulmonary smooth muscle cells are BKα-β₁ functional complexes lacking the oxygen-sensitive stress axis regulated exon insert.

ABSTRACT: A loss of K⁺ efflux in pulmonary arterial smooth muscle cells (PASMCs) contributes to abnormal vasoconstriction and PASMC proliferation during pulmonary hypertension (PH). Activation of high-conductance Ca²⁺-activated (BK) channels represents a therapeutic strategy to restore K⁺ efflux to the affected PASMCs. However, the properties of BK channels in PASMCs-including sensitivity to BK channel openers (BKCOs)-are poorly defined. The goal of this study was to compare the properties of BK channels between PASMCs of normoxic (N) and chronic hypoxic (CH) rats and then explore key findings in human PASMCs. Polymerase chain reaction results revealed that 94.3% of transcripts encoding BKα pore proteins in PASMCs from N rats represent splice variants lacking the str

SUBMITTER: Detweiler ND

PROVIDER: S-EPMC5210062 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Dataset Information

BK channels in rat and human pulmonary smooth muscle cells are BKα-β₁ functional complexes lacking the oxygen-sensitive stress axis regulated exon insert.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

BK channels in rat and human pulmonary smooth muscle cells are BKα-β1 functional complexes lacking the oxygen-sensitive stress axis regulated exon insert.

OmicsDI is part of the ELIXIR infrastructure

Tweets

BK channels in rat and human pulmonary smooth muscle cells are BKα-β₁ functional complexes lacking the oxygen-sensitive stress axis regulated exon insert.