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Regulation of aldose reductase expression in rat astrocytes in culture
Author(s) -
JacquinBecker and Clarisse,
Labourdette Gérard
Publication year - 1997
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(199706)20:2<135::aid-glia5>3.0.co;2-8
Subject(s) - astrocyte , biology , aldose reductase , basic fibroblast growth factor , epidermal growth factor , fibroblast growth factor , extracellular , neuroglia , endocrinology , medicine , cell culture , downregulation and upregulation , growth factor , fibroblast , aldose reductase inhibitor , microbiology and biotechnology , biochemistry , receptor , central nervous system , diabetes mellitus , genetics , gene
Aldose reductase (AR) is known to be responsible for many side effects of diabetes. In the present work, we studied the effects of various extracellular signals on the regulation of the expression of AR in astrocytes in culture, by determining its enzymatic activity or its mRNA level. We found that basic fibroblast growth factor (bFGF), acidic fibroblast growth factor (aFGF), epidermal growth factor (EGF), and hypertonic NaCl were able to increase the expression of AR in astrocytes. A superinduction was found when bFGF was combined with hypertonicity. We also observed that AR activity was independent of glucose concentration in the culture medium. However, when the concentration of glucose in the culture medium was under 1 g/l, bFGF did not increase the activity of AR. Thus, when glucose is depleted, the regulation of AR expression by bFGF does not operate. In addition, AR does not seem to be involved in control of astrocyte proliferation, in contrast to the effects reported on other cell types. These results indicate that AR is expressed in astrocytes and that its expression is upregulated by hypertonicity but also by FGFs and EGF. This suggests that in these cells, AR elicits some regulatory functions. GLIA 20:135–144, 1997. © 1997 Wiley‐Liss Inc.