TY - JOUR
T1 - Induction of platelet-derived growth factor β-receptor in focal ischemia of rat brain
AU - Iihara, Koji
AU - Sasahara, Masakiyo
AU - Hashimoto, Nobuo
AU - Hazama, Fumitada
PY - 1996
Y1 - 1996
N2 - Our previous study on the ischemia-induced expression of platelet- derived growth factor (PDGF)-B chain in the rat brain prompted us to examine expression of PDGF β-receptor in the ischemic brain. Focal ischemia was induced by permanent tandem occlusion of middle cerebral and common carotid arteries in spontaneously hypertensive rats. Northern analysis revealed that ischemia significantly increased expression of the receptor in the ischemic neocortex at 4 and 7 days (328 ± 109%; 323 ± 119%, respectively, over control: n = 4, p < 0.05 versus sham). Neurons in infarct transiently showed increased immunostaining for the receptor at 1 day, whereas neurons in periinfarct area showed sustained and increased immunoreactivity from 1 to 14 days post-ischemia. Reactive glial cells in the external capsule and in molecular layer of the neocortex adjacent to infarct possessed enhanced immunoreactivity from 1 to 21 days. Furthermore, marked immunoreactivity was observed on brain macrophages in infarct and on the abluminal side of capillaries surrounding infarct from 4 to 7 days. These results demonstrated that ischemic insult increases expression of the PDGF β-receptor at both the mRNA and protein lever in the brain, suggesting its important role in cellular cascade of the ischemic brain.
AB - Our previous study on the ischemia-induced expression of platelet- derived growth factor (PDGF)-B chain in the rat brain prompted us to examine expression of PDGF β-receptor in the ischemic brain. Focal ischemia was induced by permanent tandem occlusion of middle cerebral and common carotid arteries in spontaneously hypertensive rats. Northern analysis revealed that ischemia significantly increased expression of the receptor in the ischemic neocortex at 4 and 7 days (328 ± 109%; 323 ± 119%, respectively, over control: n = 4, p < 0.05 versus sham). Neurons in infarct transiently showed increased immunostaining for the receptor at 1 day, whereas neurons in periinfarct area showed sustained and increased immunoreactivity from 1 to 14 days post-ischemia. Reactive glial cells in the external capsule and in molecular layer of the neocortex adjacent to infarct possessed enhanced immunoreactivity from 1 to 21 days. Furthermore, marked immunoreactivity was observed on brain macrophages in infarct and on the abluminal side of capillaries surrounding infarct from 4 to 7 days. These results demonstrated that ischemic insult increases expression of the PDGF β-receptor at both the mRNA and protein lever in the brain, suggesting its important role in cellular cascade of the ischemic brain.
UR - http://www.scopus.com/inward/record.url?scp=0029746257&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029746257&partnerID=8YFLogxK
U2 - 10.1097/00004647-199609000-00018
DO - 10.1097/00004647-199609000-00018
M3 - Article
C2 - 8784238
AN - SCOPUS:0029746257
SN - 0271-678X
VL - 16
SP - 941
EP - 949
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
IS - 5
ER -