1. Control of vascular smooth muscle cell growth by connexin 43
- Author
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Chintamani N Joshi, Chaitanya Madamanchi, David A. Tulis, Patti R. Shaver, Barbara J. Muller-Borer, and Danielle N Martin
- Subjects
Cell signaling ,medicine.medical_specialty ,Vascular smooth muscle ,Physiology ,Connexin ,030204 cardiovascular system & hematology ,Biology ,lcsh:Physiology ,03 medical and health sciences ,0302 clinical medicine ,vascular ,Internal medicine ,Physiology (medical) ,cAMP ,medicine ,vascular smooth muscle cells ,Protein kinase C ,030304 developmental biology ,Original Research ,0303 health sciences ,protein kinases ,lcsh:QP1-981 ,Cell growth ,VSMC ,Gap junction ,Cell cycle ,Cell biology ,Cx43 ,cGMP ,Endocrinology ,cardiovascular system ,Phosphorylation - Abstract
Connexin 43 (Cx43), the principal gap junction protein in vascular smooth muscle cells (VSMCs), regulates movement of ions and other signaling molecules through gap junction intercellular communication (GJIC) and plays important roles in maintaining normal vessel function; however, many of the signaling mechanisms controlling Cx43 in VSMCs are not clearly described. The goal of this study was to investigate mechanisms of Cx43 regulation with respect to VSMC proliferation. Treatment of rat primary VSMCs with the cAMP analog 8Br-cAMP, the soluble guanylate cyclase (sGC) stimulator BAY 41-2272 (BAY), or the Cx inducer diallyl disulfide (DADS) significantly reduced proliferation after 72 h compared to vehicle controls. Bromodeoxyuridine uptake revealed reduction (p
- Published
- 2012