Increased basic fibroblast growth factor immunoreactivity in the brain of stroke-prone spontaneously hypertensive rats.
To obtain information about changes of basic fibroblast growth factor (bFGF) in the brain under a chronic hypertensive condition, we immunohistochemically studied the distribution and level of bFGF in the brain of stroke-prone spontaneously hypertensive rats (SHRSPs). The advanced cerebral lesions in SHRSPs demonstrated massive bleeding, cavity formation and diffuse degeneration of the white matter, whereas the early changes were petechiae, edema and massive glial accumulation around fibrin deposition containing necrotized microvessels. In the control normotensive rats, immunoreactivity for bFGF was demonstrated in nerve cells, especially in selective neuronal populations, ependymal cells and epithelial cells of the choroid plexus, while there was almost no reactivity in astrocytes. In SHRSPs, on the other hand, there was marked immunoreactivity in the densely accumulated reactive cells, particularly astrocytes, in and around cerebral cortical lesions. Slightly increased reaction for bFGF was found in the nerve cells around lesions. Astrocytes in the subcortical white matter on both ipsi- and contralateral sides of the cortical lesion also showed immunoreactivity for bFGF. The location of increased bFGF expression in SHRSPs corresponded very well with the site of extravasated plasma fluid demonstrated by anti-fibrinogen antibody. Electron microscopically, bFGF was shown in astrocytes along the rough endoplasmic reticulum, suggesting that the growth factor was produced in the cells and not taken up from the surroundings. These findings indicate the possibility that edema and the simultaneously generated free radicals or some extravasated plasma components express bFGF in astrocytes and probably in nerve cells, and that the thus expressed bFGF plays some role in the sequence of developmental events of hypertensive cerebral lesions.
Kataoka
H
H
Department of Pathology, Shiga University of Medical Science, Otsu, Japan.
Yamada
E
E
Hazama
F
F
D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D005340:Fibrinogen / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism* / Q000473:pathology; D007124:Immunoenzyme Techniques; D008297:Male; D016253:Microscopy, Immunoelectron; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
D005904:Glial Fibrillary Acidic Protein; D016222:Fibroblast Growth Factor 2; D005340:Fibrinogen