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- W2273467900 abstract "A1 adenosine receptor (A1AR) is coupled to Gi/Go proteins, inhibiting adenylate cyclase, but the downstream signaling pathway in smooth muscle cells is unclear. Present study was performed in coronary artery smooth muscle cells (CASMC) from WT and A1AR KO mice to determine the role of protein kinase C (PKC) pathway in A1AR signaling. We used CASMC isolation method from our lab (Teng et al 2006, Am J Physiol Heart Circ Physiol. 290:H1713–20). To detect PKC isoforms, cytosolic and membrane fractions were made from cell homogenates. PKC isoforms were identified by Western blotting. In both WT and A1AR KO, basal levels of PKC α, β, γ, δ, θ, were abundant in cytosolic, and of PKC μ, ε, λ in membrane fractions whereas PKCζ was equal in both fractions. In WT cells treated with A1AR agonist, ENBA (10−5M) increased A1AR expression by 162%, and this was inhibited by 55% compared with control by A1AR antagonist DPCPX (10−6M), whereas there was no effect in A1AR KO. In WT, ENBA activated PKCα expression by 190% over control, and it was inhibited by specific PKCα inhibitor Gö6976 (10−7M), but unchanged in A1AR KO (p<0.05). In organ bath experiments, Gö6976 (10−7M) inhibited ENBA-induced aortic contraction by 45% in WT, but no effect was noted in A1AR KO. The phospholipase C (PLC) inhibitor U73122 (10−6M) reduced the expression of PLCγ and pERK1/2 by 54% and 51%, respectively (p<0.05). We conclude that A1AR activation by ENBA activates PLC, mainly through PKCα leading to ERK1/2 phosphorylation and contraction in CASMC. Supported by HL-027339." @default.
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- W2273467900 date "2008-03-01" @default.
- W2273467900 modified "2023-09-25" @default.
- W2273467900 title "A1 adenosine receptor‐activated protein kinase C signaling in A1 knock‐out mice coronary artery smooth muscle cells" @default.
- W2273467900 doi "https://doi.org/10.1096/fasebj.22.1_supplement.1152.11" @default.
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