Study Of Different Expressions Of NOGO-B In Atherosclerosis Lesion

Atherosclerosis is not merely a disease in its own case, but a process that is the principal contributor to the pathogenesis of myocardic infarction and cerebral stroke, extremities gangrene. Despite the universal occurrence of atherosclerosis in the world, the pathogenesis of disease remains incompletely understood. In the injury theory of R.Ross, atherosclerosis can be considered to be a modified form of chronic inflammation induced by lipids, and many have followed in this path.During the early stage of atherosclerosis, there are normally damaging and exfoliating of endothelium cells, lipoprotein entering into the intima of the artery, proliferating of smooth muscle cells and developing into foam cells. Finnally the atherosclerosis lesions are formed. It is said that the damaged endothelium cells are the initiation factors. During the early period time of atherosclerosis, the lipid of plaque is coming from oxidized low density lipoprotein. Although many cells in the lesion can all oxidize low density lipoprotein, the endothelium cells play an important role.NOGO is a type of transmembrane protein, having three main subtypes (NOGO-A, B, C). Recently many studies are focusing on the biology function, receptors and the inhibition to axonal growth and regeneration of NOGO-A. NOGO-B is found in many tissue, especially in vessles. Researches have showed that NOGO-B inhibited the regeneration of vessle. In our study, lysophosphatidyl choline incubated with mouse heart microvascular endothelium cells, in order to mimic the pathologic change of atherosclerosis, and atherosclerosis rat models had been developped. NOGO-B was detected in these models, so did in the tissue of aortic desection patients.The different expression of NOGO-B in AS lesion and non-AS lesion , and of the subtypes of NOGO-B.The progress of this study were presented in three parts:1.The expressions of NOGO-B in normal H5V cells and H5V cells incubated with LPC.1) Detecting with Western Blotting, N0G0-B1 protein was found expressing in normal H5V cells but no NOGO-B2 was found, while the mRNA of both subtypes were found expressed.2) After incubated with LPC the expression level of NOGO-B1 protein in H5V cells decreased, accompany with no decreasing of mRNA expression except the 50% off on the point of 20 u M LPC at 24 hours.3) The level of protein and mRNA of NOGO-B2 in H5V cells incubated with LPC shew a transient increase.2. Raising the model of AS rats and detecting the expression of NOGO-B1) The level of NOGO-B 1 mRNA fell down while no change of NOGO-B2 in the AS lesion of rats were detected by Nothern Blotting method.2) The expression of NOGO-B decreased in the AS lesion especially in the intima of aorta by immunohistochemistry method.3. Detecting the expression of NOGO-B in the tissue of 3 aortic desection patients1) The expession level of NOGO-B in the intima of AS lesion of human aorta decreased by Western Blotting.2) The expession level of NOGO-B in the intima of AS lesion of humanaorta decreased , which was confirmed by immunohistochemistry method. Conclusion: NOGO-B participated the formation of atherosclerosis lesion. During the period of atherosclerosis, the expression level of NOGO-B2 shew a transient change, while the expression level of NOGO-B 1 decreased.