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Connexin isoform expression in microvascular smooth muscle and endothelium
Author(s) -
Hakim Chady,
Jackson William F.,
Segal Steven S.
Publication year - 2007
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.21.6.a1217-c
Subject(s) - gene isoform , connexin , immunolabeling , microbiology and biotechnology , cheek pouch , gap junction , biology , endothelium , anatomy , cell , hamster , chemistry , immunohistochemistry , biochemistry , intracellular , gene , endocrinology , immunology
Endothelial cells (EC) have been implicated in providing the pathway for conducted vasodilation. A complementary role for smooth muscle cells (SMC) remains controversial, in part due to lack of quantitative measurements of Cx expression in respective cell layers. Our goal here was to quantify the expression of Cx isoforms in EC and SMC from hamster cheek pouch arterioles (CPA) and retractor feed arteries (RFA). Microvessels were dissected, dissociated, and SMC (300–400 cells) or EC (6–10 tubes) were collected to generate cDNA. Following reverse transcription, qRT‐PCR was performed for Cx37, Cx40, Cx43, PECAM‐1 and smooth muscle α‐actin (SMAA). Transcript copy numbers were similar for each Cx isoform in EC from CPA and RFA (~0.5 Cx/PECAM‐1) and relatively higher (P<0.05) than those in SMC (<0.1 Cx/SMAA). In contrast, Cx43 transcript in SMC from small intestine approached levels in EC (~0.4 Cx43/SMAA). Punctate immunolabeling for Cx was robust at cell borders of EC tubes and intestinal SMC but undetectable in SMC of CPA or RFA. We conclude that EC are the principal site of Cx expression in CPA and RFA. Low Cx expression in SMC may reflect discrete homocellular and myoendothelial gap junctions. (Support: HL41026, HL56786, HL32469).