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Regulation of voltage‐gated calcium channel expression by estrogen
Author(s) -
Dalton Jamie,
Joseph Biny K.,
Rusch Nancy J.,
Hill Brent J.F.
Publication year - 2010
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.24.1_supplement.985.7
Subject(s) - vasoconstriction , estrogen , medicine , voltage dependent calcium channel , vascular smooth muscle , endocrinology , calcium channel , endothelium , coronary artery disease , coronary arteries , calcium , blot , chemistry , cardiology , artery , smooth muscle , biochemistry , gene
We previously demonstrated that a physiological estrogen (E2) concentration decreases the protein expression of the voltage‐gated calcium channel (VGCC) pore‐forming α 1C subunit in coronary arteries. However, it is not known how E2 elicits this effect. In this study we hypothesized that the E2 mediated down‐regulation occurs via a posttranscriptional pathway in arterial smooth muscle. Right coronary arteries were obtained from hearts of mature sows. The distal end of the artery was cut into longitudinal strips, and the endothelium was left intact or mechanically removed. The strips were incubated for 24 hours in E2 (1 nM) or its ethanol solvent. Using RT‐PCR our data suggest that E2 has no effect on the mRNA expression of the VGCC α1C subunit. Preliminary results from Western blots indicate that the decrease in VGCC expression by E2 is endothelium‐independent. Our findings provide important insights into the mechanistic pathway of the E2 mediated down‐regulation of VGCCs. Because vascular disease is accompanied by endothelial damage, the presence of circulating E2 may have beneficial effects to limit coronary vasoconstriction. Support: NCRR of the NIH, Grant #P20 RR‐16460