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Article type: Research Article
Authors: Sakaguchi, Tateo | Yamada, Kazuo | Wanaka, Akio | Kohmura, Eiji | Yuguchi, Takamichi | Taneda, Mamoru | Kataoka, Kazuo | Tohyama, Masaya | Hayakawa, Toru
Affiliations: Department of Neurosurgery, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan | Department of Anatomy and Neuroscience, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan | Department of Neurosurgery, Kinki University School of Medicine, Osaka, Japan
Note: [] Corresponding author. Tel.: 81 6 879 5111; Fax: 81 6 879 3659.
Abstract: The present study examined whether expression of basic fibroblast growth factor receptor (bFGFR) messenger ribonucleic acid (mRNA) was upregulated by focal ischemia. We have studied the in situ hybridization autoradiography for bFGFR mRNA in the rat model of middle cerebral artery (MCA) occlusion. Male Wistar rats were used for occlusion of the left MCA, and were sacrificed 1, 3, 7 and 14 days after MCA occlusion. In situ hybridization was performed on the brain sections of these animals and sham controls by using 35S-labeled antisense and sense (control) RNA probes for rat bFGFR. Expression of bFGFR mRNA was observed in the periinfarcted area of the rats within 1-14 days after MCA occlusion. Expression was evident in the whole hemisphere of the infarcted side, especially at 1 and 3 days after ischemia, but no expression was detected in the contralateral side. On microautoradiograms, the signals of bFGFR mRNA were detected in both neurons and non-neural cells located in the periinfarcted area. Upregulation of bFGFR mRNA detected in the periinfarcted brain tissue suggests that receptor-mediated action of bFGF may be related to preservation of neurons injured by ischemia.
Keywords: In situ hybridization, Fibroblast growth factor, Receptor, Focal ischemia, Cerebral infarction, Autoradiogram
DOI: 10.3233/RNN-1994-7105
Journal: Restorative Neurology and Neuroscience, vol. 7, no. 1, pp. 29-36, 1994
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