TY - JOUR
T1 - Expression of platelet-derived growth factor after transient forebrain ischemia in the gerbil hippocampus.
AU - Kaneko, M.
AU - Sasahara, M.
AU - Takayama, S.
AU - Handa, J.
AU - Hazama, F.
N1 - Funding Information:
Acknowledgements We thank Dr. T. Matsui (Kobe University, Japan) for the cDNA probes for PDGFR-a , Dr. R. G. K. Gronwald (University of Washington, Seattle, Wash.) for PDGFR-b , and Dr. C. H. Heldin (Ludwig Institute for Cancer Research Biomedical Center, Uppsala, Sweden) for PDGF-A. We wish to thank the Mochida Pharmaceutical Company (Tokyo, Japan) for supplying the monoclonal antibody PGF-007. We also thank Ms. S. Hi-rayama for excellent technical assistance. This work was supported in part by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture of Japan (#06670223, #08670246).
PY - 1998/5
Y1 - 1998/5
N2 - The present study was conducted to clarify the role of platelet-derived growth factor-B chain (PDGF-B) in neuronal death after ischemia. Transient forebrain ischemia was induced in Mongolian gerbils by occluding the bilateral carotid arteries for 5 min. We investigated PDGF-B expression in the hippocampus after ischemia by immunohistochemistry, Northern blotting and in situ hybridization histochemistry. The results showed that PDGF-B is expressed in control CAI and CA3 neurons. In CA1, the amount of the PDGF-B transcript immediately increased, then disappeared 2 days after ischemia. Delayed neuronal death followed 1 day later. However, PDGF-B immunoreactivity in CA1 rapidly decreased and disappeared 12 h after transient forebrain ischemia, proceeding to delayed neuronal death. In contrast, the expression of both PDGF-B protein and the transcript was well preserved throughout the study in CA3, which remained viable even after ischemia. Accordingly, the selective neuronal susceptibility in the CA1 to ischemia corresponded with rapid disappearance of PDGF-B. PDGF-B expression may contribute to neuroprotective effect after ischemia.
AB - The present study was conducted to clarify the role of platelet-derived growth factor-B chain (PDGF-B) in neuronal death after ischemia. Transient forebrain ischemia was induced in Mongolian gerbils by occluding the bilateral carotid arteries for 5 min. We investigated PDGF-B expression in the hippocampus after ischemia by immunohistochemistry, Northern blotting and in situ hybridization histochemistry. The results showed that PDGF-B is expressed in control CAI and CA3 neurons. In CA1, the amount of the PDGF-B transcript immediately increased, then disappeared 2 days after ischemia. Delayed neuronal death followed 1 day later. However, PDGF-B immunoreactivity in CA1 rapidly decreased and disappeared 12 h after transient forebrain ischemia, proceeding to delayed neuronal death. In contrast, the expression of both PDGF-B protein and the transcript was well preserved throughout the study in CA3, which remained viable even after ischemia. Accordingly, the selective neuronal susceptibility in the CA1 to ischemia corresponded with rapid disappearance of PDGF-B. PDGF-B expression may contribute to neuroprotective effect after ischemia.
UR - http://www.scopus.com/inward/record.url?scp=0032065993&partnerID=8YFLogxK
U2 - 10.1007/s004010050827
DO - 10.1007/s004010050827
M3 - 学術論文
C2 - 9600593
AN - SCOPUS:0032065993
SN - 0001-6322
VL - 95
SP - 471
EP - 478
JO - Acta Neuropathologica
JF - Acta Neuropathologica
IS - 5
ER -