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TGF‐β1–dependent differential expression of a rat homolog for latent TGF‐β binding protein in astrocytes and C6 glioma cells
Author(s) -
Krohn Knut
Publication year - 1999
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(19990215)25:4<332::aid-glia3>3.0.co;2-1
Subject(s) - biology , differential display , downregulation and upregulation , transforming growth factor , transforming growth factor beta , microbiology and biotechnology , microglia , gene expression , gene , immunology , genetics , inflammation
Transforming growth factor‐β1 (TGF‐β1) is widely recognized for its multiple roles in development, cellular maintenance, and protection against injury. In the brain, TGF‐β1 upregulation in microglia/macrophages is a predominant response to lesion and during pathology. However, the precise functions of TGF‐β1 in this context are still enigmatic. The present study investigates changes in astroglial gene expression as a major target of TGF‐β1 signaling in the brain. Differential display reverse transcription‐polymerase chain reaction (DDRT‐PCR) was used to identify several gene fragments differentially regulated by TGF‐β1 in rat astrocytes and C6 glioma cells. Among the cDNAs regulated by TGF‐β1 in C6 cells two cDNAs showed homology to α‐tropomyosin and glycerol‐3‐phosphate dehydrogenase, respectively. Cloning of a full length cDNA corresponding to a differentially regulated gene fragment revealed close homology to latent TGF‐β binding protein (LTBP)‐2. Data using antisense LTBP‐2 oligonucleotides to decrease LTBP‐2 expression suggest that LTBP‐2 functions to activate TGF‐β. Therefore, it is likely that upregulation of the rat LTBP‐2 homolog mRNA in C6 cells and cortical astrocytes by TGF‐β1 might lead to self‐activation and exaggeration of TGF‐β signaling. These data will extend our current understanding of TGF‐β1 functioning on lesion‐related features of glial cells. GLIA 25:332–342, 1999. © 1999 Wiley‐Liss, Inc.