The Investigation Of The Relationship Between The MarburgⅠ Polymorphism Of FSAP And Cerebral Infarction

Objective: The factorⅦ-activating protease (FSAP) is a novel plasma-derived serine protease, which consists of three epidermal growth factor (EGF)-like domains, a kringle domain, and a serine protease domain. The Marburg I polymorphism of FSAP locating in the serine protease domain results in significant impairment not only in the pro-urokinase activating potency, but also in the proteolysis potency of FSAP to the platelet- derived growth factor-BB (PDGF-BB), the basic fibroblast growth factor (bFGF) and the vascular endothelial growth factor (VEGF). As a result, the inhibitory action of FSAP to these cytokine-mediated proliferation and migratation of the vascular smooth muscle cell (VSMC) and the endothelial cell will be weakened. All the functional impairment will accelerate the development of angiosclerosis and arterial stenosis process.There are a number of aboard reports characterized that the Marburg I polymorphism of FSAP is related with a wide variety of thrombus diseases. As a thrombus-related disease, cerebral infarction's main pathological changes is the formation of vascular thrombosis on the basis of the cerebral arteriosclerosis, which block blood flow and result in brain ischemia, hypoxia and necrosis. And the functional impairment of the FSAP Marburg I mutant can cause or aggravate these pathologic processes in theory. However, there is no research about the relationship between FSAP Marburg I polymorphism and cerebral infarction. Our object is the first time to explore the clinical relationship between FSAP Marburg I polymorphism and cerebral infarction, and analysis whether it is one of the risk factors of cerebral infarction.Methods: The single strand conformation polymorphism-polymerase chain reaction (SSCP-PCR) was employed for the polymorphism analysis of FSAP gene in patients with cerebral infarction and age,sex matched volunteers without thrombus-related diseases history. The Fisher probabilities in 2×2 table was employed for the statistical analysis.Results: The phenotypes of FSAP in both patients group and control group were wild type of GG, no mutant of Marburg I was found. But a additional gene mutation was identified in the samples tested, which has not been reported. It needs to be further researched about the functional alteration of this gene mutation.Conclusion: There may be no correlation between FSAP Marburg I polymorphism and cerebral infarction.