Tyrosine kinase signaling involved in glutamate-induced astrocyte proliferation.
Proliferation of astrocytes is a common response of the CNS to injury and disease. The mechanisms controlling the proliferation of astrocytes are of great interest. In this paper, the signaling pathways underlying glutamate-induced astrocyte proliferation are investigated. Glutamate stimulates the proliferation of non-synchronized, subconfluent cultures of rat cortical astrocytes. Glutamate-induced cell proliferation is not prevented by inhibitors of G protein, protein kinase A, protein kinase C, phosphatidylinositol 3 kinase, extracellular signal-regulated kinase, or phospholipase A2. However, the tyrosine kinase inhibitors Genistein and Herbimycin A inhibit the glutamate-induced proliferation. Moreover, this proliferation is mediated by the activation of glutamate metabotropic receptors. These results suggest that glutamate induces astrocyte proliferation through a tyrosine kinase pathway.
Liao
S L
SL
Department of Education and Research, Taichung Veterans General Hospital, No. 160, Sec. 3, Taichung-Gang Rd., Taichung 40705, Taiwan, Republic of China.
Chen
C J
CJ
D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology*; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D018698:Glutamic Acid / Q000494:pharmacology*; D011505:Protein-Tyrosine Kinases / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*
D018698:Glutamic Acid; D011505:Protein-Tyrosine Kinases