This study has demonstrated a role for MyD88-dpendent signalling in the response to MCAO further work to understand the location and particular pathways involved will significantly extend the field of neuro-immuno-biology. Brain arteriovenous malformations are relatively infrequent but important sources of spontaneous intracranial hemorrhage and may cause a life-threatening ICH in 2�C6% of cases annually, which would result in high neurological morbidity in young adults. Although most discovered BAVMs can be treated by some combination of surgical resection, endovascular embolization and radiosurgery, patients with typical BAVMs of high Spetzler-Martin grade are still facing huge therapeutic risks. The genesis of AVMs is still unclear, but several gene mutations, such as ALK-1 variants, have been associated with a risk of sporadic BAVM. BAVMs are often presumed to be congenital, but there is little direct evidence to support this idea. However, recent studies indicate that BAVMs can grow or regress after birth due to active angiogenesis. Because post-natal growth is possible and even likely, one plausible basis for therapy would be further slow this already very slow growth over time.Based on the existing literature, we hypothesized that BAVMs could arise congenitally due to specific gene mutations and could also be stimulated by some post-natal events. The inciting events might include subclinical injury from otherwise unremarkable episodes of trauma, infection, inflammation, irradiation or compression. Then, VEGF and other inflammation factors activate angiogenesis, followed by the excessive degradation of the vascular matrix by matrix metalloproteinase. MMPs comprise a family of proteolytic enzymes that degrade extracellular matrix proteins, cell surface molecules and other pericellular substances, which may result in the destabilization of vessels. This is a critical step in further angiogenesis and vascular remodeling. It appears that histological prototype of BAVM, which is called vascular dysplasia is developed after this event. The basic morphology of a mature BAVM is a vascular mass, called the nidus, which is a complex tangle of abnormal, dilated channels that are not clearly arterial or venous, with intervening gliosis that directly shunts blood between the arterial and venous circulations without a true capillary bed. Thus, we suggest that abnormal vascular remodeling, mainly stimulated by MMPs, is more important in BAVM development. The increased expression of MMPs in BAVM tissues have been confirmed, and MMP3 is an crucial activator of a number of proMMPs. In vitro, endothelial cell proliferation and migration could be affected by elevated MMP3. In our previous case-control study, we found that a single nucleotide polymorphism rs522616 A.G variant of the MMP3 promoter was significantly associated with BAVM in a Chinese Han population. Logistic regression analysis revealed that the variant genotype G was associated with a significantly decreased risk of BAVM. This finding indicated that the MMP3 rs522616 polymorphism may contribute to the etiology of sporadic BAVM in the Chinese Han population. However, the relationship between the rs522616 polymorphisms and the expression of MMP3 remains unclear. In this study, we compared the transcriptional activities of the MMP3 promoters with A or G alleles to determine the molecular biological effects of the MMP3 rs522616 polymorphism.

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