TGFβ1 selectively up-regulates CCR1 expression in primary murine astrocytes

✍ Scribed by Yulong Han; Jintang Wang; Z.-H. Lucy Zhou; Richard M. Ransohoff

• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 246 KB
• Volume: 30
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/(sici)1098-1136(200003)30:1<1::aid-glia1>3.0.co;2-q

✦ Synopsis

Chemokine receptors dictate the cellular responses to chemokines on target cells. Therefore, the regulation of expression of chemokine receptors is likely a crucial point for the regulation of chemokine action. Here we show that CC chemokine receptor 1 (CCR1) expression by primary mouse astrocytes is increased after transforming growth factor ␤1 (TGF␤1) stimulation. TGF␤1 caused a pronounced up-regulation of CCR1 mRNA in a concentration-and time-dependent manner. TGF␤1-mediated increase of CCR1 mRNA accumulation resulted in increased CCR1 protein expression and augmented cell migration to a physiological ligand, macrophage inflammatory protein-1␣ (MIP-1␣). The half life of CCR1 mRNA in the presence and absence of TGF␤1 stimulation was comparable, suggesting that TGF␤1-induced CCR1 mRNA accumulation occurred at the transcriptional level. TGF␤1 did not affect CCR1 mRNA expression in hematopoietic cells, indicating that TGF␤1 effect on CCR1 expression in primary astrocytes is cell-type specific. This is the first evidence that TGF␤1 may modulate central nervous system (CNS) inflammation in part by affecting chemokine receptor expression on astrocytes. GLIA 30: 1-10, 2000.