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Decreased Expression of VEGF‐A in Rat Experimental Autoimmune Encephalomyelitis and in Cerebrospinal Fluid Mononuclear Cells from Patients with Multiple Sclerosis
Author(s) -
Tham E.,
Gielen A. W.,
Khademi M.,
Martin C.,
Piehl F.
Publication year - 2006
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2006.01851.x
Subject(s) - experimental autoimmune encephalomyelitis , pathogenesis , multiple sclerosis , cerebrospinal fluid , vascular endothelial growth factor , angiogenesis , in situ hybridization , encephalomyelitis , neuroinflammation , medicine , immunology , receptor , pathology , central nervous system , peripheral blood mononuclear cell , biology , messenger rna , vegf receptors , inflammation , cancer research , endocrinology , gene , biochemistry , in vitro
Vascular endothelial growth factor A (VEGF‐A) stimulates angiogenesis, but is also pro‐inflammatory and plays an important role in the development of neurological disease, where it can have both attenuating and exacerbating effects. VEGF‐B, a related molecule, is highly expressed in the central nervous system and seems to be important in neurological injury. A few studies have indicated that VEGF‐A may play a role in the pathogenesis of multiple sclerosis (MS), but the role of VEGF‐B has not been studied. We have studied the expression of VEGF‐A, ‐B and their receptors by mRNA in situ hybridization, immunohistochemistry and real‐time PCR in spinal cord from LEW rats with experimental autoimmune encephalomyelitis (EAE) and in cerebrospinal fluid (CSF) and blood samples from MS patients. Whereas VEGF‐A is downregulated in glia in EAE, the infiltrating inflammatory cells are positive for VEGF‐A. Expression of VEGF‐B and the VEGF receptors is unaltered. In addition, the levels of VEGF‐A mRNA in monocytes in CSF are lower in MS patients compared with controls. These results demonstrate a complex regulation of VEGF‐A during neuroinflammation and suggest that VEGF‐B is not involved in the pathogenesis of MS.