Post traumatic lesion absence of beta-dystroglycan-immunopositivity in brain vessels coincides with the glial reaction and the immunoreactivity of vascular laminin.
Following brain lesions, the gliovascular basal lamina undergoes destruction and the gliovascular connections 'decouple'. Laminin receptors, as dystroglycan, are essential in these processes. The present study compares the immunoreactivities of beta-dystroglycan, glial fibrillary acidic protein (GFAP), and laminin following stab wounds in adult rats. In intact brain the vessels were immunopositive to beta-dystroglycan, whereas the laminin of their basal lamina proved to be unavailable to immunoreactions. Following stab wound, however, the adjacent vessels lost their immunopositvity to beta-dystroglycan, whereas immunopositivity to laminin became detectable in them. In an advanced stage of glial reaction the territory of GFAP immunopositive reactive astrocytes coincided with the area where vessels lost their immunopositivity to beta-dystroglycan. When glial reaction regressed, the beta-dystroglycan immunopositivity re-appeared, and laminin immunopositivity became undetectable again. Post-lesional disappearance of vascular beta-dystroglycan immunostaining was described earlier, and was attributed to the cleavage of beta-dystroglycan by matrix metalloproteinases as a mechanism of the decoupling of the gliovascular connections. Our results, which were obtained in a different type of lesion support that the loss of vascular beta-dystroglycan immunopositivity is a general phenomenon following cerebral lesions, and an indirect marker of gliovascular decoupling. For the first time coincidences were presented between vascular immunonegativity to beta-dystroglycan, glial reaction and detectability of laminin. Manifestation of laminin immunoreactivity also indicates gliovascular decoupling. Coincidence between glial reaction and lack of vascular beta-dystroglycan suggests mutual enhancement between them. The observations may have clinico-pathologic importance since similar investigations may help to follow the progression and regression of post-lesion processes.
Szabó
Adrienn
A
Department of Anatomy, Semmelweis University, Budapest, Hungary.
Kálmán
Mihály
M
D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001485:Basement Membrane / Q000378:metabolism* / Q000473:pathology; D001929:Brain Edema / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002536:Cerebral Arteries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D018450:Disease Progression; D049030:Dystroglycans / Q000276:immunology / Q000378:metabolism*; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D007797:Laminin / Q000276:immunology / Q000378:metabolism*; D008297:Male; D051381:Rats
D005904:Glial Fibrillary Acidic Protein; D007797:Laminin; D049030:Dystroglycans