The Role Of RYR3?MiR-29b And MMP-9 In The Process Of Arteriosclerosis Plaque Formation In Apolipoprotein E Gene-defici-Ent Mice

Objective:The incidence of atherosclerotic vascular disease is closely related to the activation and activation of calcium channels,the level of calcium in the vascular smooth muscle cells of apolipoprotein E gene-deficient mice increases before the formation of atherosclerotic plaques,In this study,we established an apolipoprotein E gene defect(ApoE gene-/-)atherosclerotic mouse model to observe the changes in RYR3 expression in aortic vascular smooth muscle cells and to elucidate its relationship with atherosclerosis Plaque relationship. the expression of miR-29b in AS model and normal blood vessel was compared with that of Apo-e(-/-)mouse AS(atherosclerosis,AS)model and normal control mice.Fluorescence quantitative PCR and To investigate the expression of MMP-9 in the process of AS,and to explore the relationship between the expression of miR-29b and MMP-9 in AS.METHOD:8 weeks old male,weighing 19-21g.fed to 20,27 and 33 weeks of age each group were randomly assigned to 15 killed,HF and Masson staining was performed on the aorta,and the percentage of plaque area and percentage of plaque area were calculated.The lipid content of plaque was analyzed by oil red O staining.The percentage of RYR3 positive expression was detected by immunohistochemical staining.The expression of RYR3 in vulnerable plaque formation was quantitatively analyzed by western blot.All the mice were sacrificed by 1%pentobarbital sodium 0.2?0.3 ml.The total cholesterol(TC)content in the serum of mice was determined by automatic biochemical analyzer.Take the aorta arch,the first line of general observation of the endometrium is light yellow patchy protrusions,followed by Sudan IV staining to observe the formation of endometrial fat pattern,the last line MASSON staining observed vascular wall fibrosis and HE staining observed foam cellsl.After the succession of AS mice induced by high fat diet,the aortic arch tissue was isolated from the sterile surgical platform,and preserved with liquid nitrogen and paraffin embedding respectively.The expression of MMP-9 protein in the blood vessels was detected by immunohistochemistry.Results:In the control group,no atherosclerotic plaque formation was observed in 20,27 and 33 week old mice,and no significant changes were observed in the middle VSMC.Masson staining showed that the size of the mice in the model group increased with the increase of age,and the fibrous tissue gradually decreased(blue),The levels of TC,TG and LDL-C in model group were significantly higher than those in control group(P<0.01),but HDL-C level was similar.RYR3 protein expression was significantly different from that of the control group(P<0.05).The expression of RYR3 protein in ApoE knockout mice was significantly higher than that in the control group(P<0.05)Masson staining showed that the NS group showed that the aorta and the medial collagen fibers were stained with light blue,indicating that the AS model was constructed successfully.The expression of MMP-9 in the FS group was significantly higher than that in the FS group(P<0.05).The expression of MMP-9 in the FS group was significantly higher than that in the FS group,suggesting that the expression of aorta in the AS model was significantly higher than that in the NS group(P<0.01)The presence of MMP-9 receptors is elevated in the intima of blood vessels.Conclusion:The level of serum cholesterol in ApoE knockout mice was significantly higher than that in the control group.TC and LDL-C levels and lipid areas also increased with age.Abnormal expression of RYR3 protein and elevated levels of lipid levels are involved in the formation of atherosclerotic plaques.Thus,RYR3 is involved in the pathogenesis of atherosclerotic plaque formation.In the atherosclerosis model of apo-E(-/-)mice with high fat diet,the expression of miR-29b in the late stage of atherosclerosis decreased and the expression of MMP-9 increased,which may be related to atherosclerotic plaque The formation of the block.