Isoform-specific role of transforming growth factor-β2 in the regulation of proliferation and differentiation of murine adrenal chromaffin cells in vivo

✍ Scribed by Belal Rahhal; Nicole Dünker; Stephanie Combs; Kerstin Krieglstein

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 345 KB
• Volume: 78
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.20286

✦ Synopsis

Abstract

Chromaffin cells, the neuroendocrine cells of the adrenal medulla, play an important role in molecular, cellular, and developmental neurobiology. Unlike the closely related sympathetic neurons, chromaffin cells are able to proliferate throughout their whole life span. Proliferation of chromaffin cells in vivo is thought to be regulated by the interaction of neurogenic and hormonal signals. Previous studies have shown that chromaffin cells synthesize and release transforming growth factor‐βs (TGF‐βs). In the present study, effects of TGF‐βs on proliferation and differentiation of chromaffin cells in mouse adrenal chromaffin cells were investigated in a genetic mouse model. We observed a significant increase in the total number of tyrosine hydroxylase‐positive (TH^+^) cells in Tgfβ2^−/−^ knockout mouse embryos at embryonic day (E) 18.5 compared with wild‐type animals (Tgfβ2^+/+^), but no changes in the number of TH^+^ cells were observed in Tgfβ3^−/−^ mouse mutants. At E15.5, but not at E18.5, there was a marked increase in the number of proliferative cell nuclear antigen‐positive chromaffin cells in Tgfβ2^−/−^ knockout embryos compared with the wild‐type group. On the other hand, there was a clear decrease in the ratio of total number of phenylethanolamine‐N‐methyltransferase‐positive cells to the total TH^+^ in Tgfβ2^−/−^ mice embryos at E18.5 compared with wild‐type animals. This is the first documentation of the physiological significance of the TGF‐β2, an isoform that has been suggested to play a role in the regulation of chromaffin cells proliferation and differentiation based on in vitro experiments. © 2004 Wiley‐Liss, Inc.