Prolactin induces proliferation of vascular smooth muscle cells through a protein kinase C-dependent mechanism

✍ Scribed by Marie D. Sauro; Nancy E. Zorn

• Publisher: John Wiley and Sons
• Year: 1991
• Tongue: English
• Weight: 719 KB
• Volume: 148
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041480116

✦ Synopsis

Abstract

The effects of prolactin (PRL) on A10 (aortic smooth muscle) cell proliferation were examined by measuring both [^3^H] thymidine incorporation and increases in cell number. PRL induced a significant proliferative response from 10^−11^ to 10^−7^ M, with optimal activity at 10^−10^ M. PRL also enhanced platelet‐derived growth factor (PDGF)‐induced proliferation. The possibility that PRL induces proliferation through a protein kinase C (PKC)‐mediated mechanism was also examined. PRL caused activation of PKC from 10^−12^ to 10^–8^ M. Antiserum to PRL, a monoclonal antibody directed against the PRL receptor and the immunosuppressive agent cyclosporine A, were able to inhibit PRL‐induced proliferation and activation of PKC. The PKC inhibitors, staurosporine, sphingosine, and 1‐(‐5‐isc‐quinoline‐sulfonyl)‐2‐methylpiperazine (H‐7) also antagonized both proliferation and PKC activation. These data strongly suggest that PRL‐induced A10 cell proliferation is mediated through the PKC pathway and that this may play a role in vascular smooth muscle cell hyperplasia, characteristic of the pathogenesis of cardiovascular diseases such as hypertension and atherosclerosis.