'Royal College of Obstetricians & Gynaecologists (RCOG)'
Abstract
Fulltext: Based on our previous demonstration of CXCR7 as the major mediator of CXCL12 signalling in cultured astrocytes, we have now characterized astrocytic CXCR7 expression in the diseased CNS and compared that to the expression of the second CXCL12 receptor, CXCR4. In the intact brain of adult rats CXCR7 and CXCR4 were expressed by GFAP-immunoreactive astrocytes forming the superficial glia limitans. Outside the glia limitans scattered and faint immunolabelling for CXCR7 and CXCR4 was present in very few additional GFAP-expressing astrocytes. In contrast to the restricted expression in the healthy CNS, a striking increase in CXCR7 expression was detectable in reactive astrocytes in rats with experimental brain infarcts (MCAO), in the spinal cord of rats with experimental autoimmune encephalomyelitis (EAE) as well as after mechanical compression. None of these pathologies was associated with substantial increases in astrocytic CXCR4 expression. Together, our findings favor the hypothesis of a crucial role of astrocytic CXCR7 in the progression of various CNS pathologies
