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Alpha1‐adrenergic receptor subtype specific activation of ERK in human primary smooth muscle cells (1065.4)
Author(s) -
Brown Kaitlyn,
Aungst Timothy,
Castro Christian,
Bommareddy Ajay,
VanWert Adam,
McCune Dan
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.1065.4
Subject(s) - mapk/erk pathway , western blot , receptor , vascular smooth muscle , adrenergic receptor , blot , microbiology and biotechnology , chemistry , downregulation and upregulation , biology , endocrinology , medicine , signal transduction , smooth muscle , biochemistry , gene
Three α 1 ‐adrenergic receptor (AR) subtypes have been cloned and characterized, the α 1A ‐,α 1B ‐, and α 1D ‐AR. Evidence suggests functional effects of receptor activation in various tissues is subtype selective. For example, ERK activation in cardiomyoctyes appears to be α 1A ‐AR dependent, and may be cardioprotective in heart failure. We examined α 1 ‐AR expression and subtype specific ERK activation in human primary arterial smooth muscle cells. Simultaneous co‐expression of all three subtypes was demonstrated by western blot, and further confirmed by RT‐PCR utilizing subtype specific primers. ERK activation was assessed by western blot. Preliminary data suggests ERK activation is blocked by α 1D ‐AR selective antagonists and is not induced by α 1A ‐AR selective agonists. If α 1A ‐AR selective agents were used in heart failure, our data would suggest that ERK activation in peripheral vasculature would be minimal, therefore mitigating concern of α 1A ‐AR mediated vascular injury as a result of therapy. However, additional subtype selective effects will need to be better defined by future studies.