Brain ischemia and expression of TGF-beta

The expression of transforming growth factor beta (TGF-B) isoforms, their r eceptors and TGF-beta -related Smad proteins in brain pathology chiefly inf arcts, is currently a matter of much interest. One key question is whether the expression of these compounds alters within glial cells, endothelial ce lls of microvessels and other cell types in the vicinity of infarcts. Studi es, both in vitro and in vivo, to identify and characterize the role of thi s peptide in ischemic conditions of the brain have been made. Immunoreactiv ities to TGF-b isoforms -beta1, -beta2 and -beta3, and TGF-beta receptor (T bR) type I and II have been observed in astrocytes, macrophages, neurons, e ndothelial cells and vascular smooth muscle cells of human brain infarcts. Evidence gathered from experimental models with middle cerebral artery (MCA ) occlusion demonstrates that several alterations occur during the evolutio n of brain infarcts with regard to the immunohistochemical expression of TG F-beta isoforms and their receptors. Increased expressions of the various i soforms and receptor types have been observed already at 6 h in neurons, mi crovascular endothelial cells, astroglial cells and inflammatory, cells. La ter on, immunopositive macrophages were seen in the infarcts. Such changes persisted even at day 7 after MCA occlusion. In conclusion, the various TGF-B isoforms and receptors seem to be involved ira the very complicated and important changes taking place in the vicinit y of brain infarcts.