Time Course, Distribution and Cell Types of Induction of Transforming Growth Factor Betas following Middle Cerebral Artery Occlusion in the Rat Brain
Figure 3
The induction of TGF-β1, - β2, and -β3 mRNA 72 h and 1 mo after MCAO.
In situ hybridization sections show the expression of TGF-β mRNA. The infarct areas are indicated by the star symbol (*) and the borders of the infarcts are demarcated with white dots. A: TGF-β1 expression is induced at the perimeter of the lesion as well as within the infarct area 72 h after MCAO. High magnification bright field photomicrographs demonstrate that TGF-β1 mRNA accumulates above cell bodies within the infarct area (Aa), as well as in the corpus callosum (Ab). The locations of these pictures are indicated by the arrowheads in the left panel. B: TGF-β2 is present in layers II, III, and V of the cerebral cortex. Only a few cells demonstrate increased expression level of TGF-β2 in the vicinity of the border of the lesion at 72 h after MCAO. C: TGF-β3 is present in some neurons in layer IV of the cerebral cortex, but the level of expression is not higher than that in normal animals D: The induction of TGF-β1 mRNA is demonstrated 1 month after MCAO. TGF-β1 mRNA is abundant within the infarct area except for in a relatively small core region. The field indicated by the large black arrowhead in A is enlarged and shown in bright-field in the inlet to demonstrate that even the densest TGF-β1 signal represents labeling of individual cells as autoradiography grains accumulated above cell bodies. E: TGF-β2 mRNA is present in a few cells at the perimeter of the infarct area. Outside the lesion, TGF-β2 mRNA is distributed in the cerebral cortex as in intact animals but is not induced above normal levels. Abbreviations: ac – anterior commissure, cc – corpus callosum, CP - caudate putamen, LV - lateral ventricle. Scale bar = 2 mm for A and E, 1 mm for C, and 50 µm for B.