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Increased expression of the neurofibromatosis 1 (NF1) gene product, neurofibromin, in astrocytes in response to cerebral ischemia
Author(s) -
Giordano M.J.,
Mahadeo D.K.,
He Y.Y.,
Geist R.T.,
Hsu C.,
Gutmann D.H.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960115)43:2<246::aid-jnr12>3.0.co;2-4
Subject(s) - neurofibromin 1 , glial fibrillary acidic protein , neurofibromatosis , ischemia , cancer research , biology , gene product , astrocyte , tumor suppressor gene , microbiology and biotechnology , brain ischemia , pathology , gene expression , neuroscience , gene , medicine , carcinogenesis , immunology , central nervous system , genetics , immunohistochemistry
Tumor suppressor genes encode proteins involved in growth regulation in differentiating and proliferating cells. Previous work from our laboratory has demonstrated that the neurofibromatosis 1 (NF1) tumor suppressor gene is dramatically upregulated in astrocytes stimulated with dibutyryl cyclic AMP and pro‐inflammatory cytokines. To explore the possibility that the NF1 gene product, neurofibromin, plays a role in the reactive gliosis seen in response to cerebral ischemia, expression of NF1 was examined in both focal and global models of rat cerebral ischemia. In this report, we demonstrate the increased expression of both neurofibromin and glial fibrillary acidic protein (GFAP) in astrocytes surrounding areas of focal ischemia. Similar increases in neurofibromin and GFAP immunoreactivity were also observed in reactive astrocytes in the hippocampal region in a global model of ischemia. These results suggest a novel role for the NF1 tumor suppressor gene in growth regulatory pathways involved in cellular remodeling and in response to injury. © 1996 Wiley‐Liss, Inc.