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Coronary artery vascular smooth muscle‐specific contractile protein expression in Syndrome X
Author(s) -
Smith Erika,
Jadhav Rashmi,
Rocic Petra
Publication year - 2009
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.23.1_supplement.775.6
Subject(s) - caldesmon , myosin , vascular smooth muscle , actin , downregulation and upregulation , western blot , medicine , artery , immunohistochemistry , alpha (finance) , chemistry , endocrinology , cardiology , anatomy , biology , smooth muscle , biochemistry , surgery , calmodulin , construct validity , patient satisfaction , gene , calcium
A key aspect of coronary collateral growth (CCG) is outward vascular remodeling. We have shown that CCG was impaired in a model of Syndrome X (JCR rat). Outward remodeling is associated with differentiated vascular smooth muscle (VSM), characterized by high VSM‐specific contractile protein expression, vs. inward remodeling, associated with de‐differentiated VSM, characterized by loss of VSM‐specific proteins. We hypothesized that expression of VSM‐specific contractile proteins was significantly lower in Syndrome X. SM‐alpha‐actin, SM‐myosin, smoothelin and caldesmon expression was evaluated by immunohistochemistry and Western blot in coronary arteries (CA) of JCR vs. healthy (WKY) rats. Results show decreased SM‐myosin (25%), SM‐alpha‐actin (50%), smoothelin (30%) and caldesmon (48%) expression in JCR vs. WKY CA. The pattern of expression differed between large (lCA) vs. small (sCA) arteries. Caldesmon was consistently lower in lCA and sCA of JCR rats, but SM‐alpha‐actin and smoothelin exhibited significantly larger decreases in sCA vs. lCA, while SM‐myosin was significantly decreased in lCA but not in sCA. These results demonstrate that coronary artery VSM is de‐differentiated in Syndrome X, but the extent of specific contractile protein downregulation differs between large vs. small coronary arteries, and may provide a partial explanation for impaired CCG in Syndrome X. NIH HL093052