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TGFβ1 selectively up‐regulates CCR1 expression in primary murine astrocytes
Author(s) -
Han Yulong,
Wang Jintang,
Zhou Z.H. Lucy,
Ransohoff Richard M.
Publication year - 2000
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(200003)30:1<1::aid-glia1>3.0.co;2-q
Subject(s) - ccr1 , biology , chemokine receptor , microbiology and biotechnology , chemokine , astrocyte , transforming growth factor , receptor , neuroscience , central nervous system , biochemistry
Abstract 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 β1 (TGFβ1) stimulation. TGFβ1 caused a pronounced up‐regulation of CCR1 mRNA in a concentration‐ and time‐dependent manner. TGFβ1‐mediated increase of CCR1 mRNA accumulation resulted in increased CCR1 protein expression and augmented cell migration to a physiological ligand, macrophage inflammatory protein‐1α (MIP‐1α). The half life of CCR1 mRNA in the presence and absence of TGFβ1 stimulation was comparable, suggesting that TGFβ1‐induced CCR1 mRNA accumulation occurred at the transcriptional level. TGFβ1 did not affect CCR1 mRNA expression in hematopoietic cells, indicating that TGFβ1 effect on CCR1 expression in primary astrocytes is cell‐type specific. This is the first evidence that TGFβ1 may modulate central nervous system (CNS) inflammation in part by affecting chemokine receptor expression on astrocytes. GLIA 30:1–10, 2000. © 2000 Wiley‐Liss, Inc.