| Background:Aortic aneurysm(AA)remains a fatal condition with high rates of morbidity and mortality,and the associated underlying mechanism influencing its pathology remains to be elucidated.Aortic aneurysm can be divided into thoracic aortic aneurysm(TAA),abdominal aortic aneurysm(AAA),or thoracic abdominal aortic aneurysm.At present,the study on aortic aneurysm mainly focuses on AAA,and its etiology and pathology can be classified into the following categories: 1)apoptosis of VSMCs;2)autophagy of cells;3)inflammation and immune response;4)an imbalance of ECM and VSMCs.However,the etiology and pathogenesis of the TAA have not been fully explained,and most of which are from the AAA conclusion.TAA and the AAA have different sources of smooth muscle cells,the thoracic aorta VSMCs are mainly derived from embryonic nerve cells,and the abdominal aorta VSMCs are mainly derived from the embryonic mesoderm and endothelial cells.In addition,the two are different in hemodynamic characteristics,risk factors,etiology and so on.All these differences prevent us from simply using the mechanism of AAA to explain the TAA.VSMCs have two phenotypes: contraction phenotype and synthetic phenotype.The contraction phenotype is fully differentiated and mature smooth muscle cells,and the aortic wall maintains its tension and integrity by contraction phenotype.It is reported that neointima,atherosclerosis and stenosis after vascular injury are all related to the phenotypic switching of VSMCs;however,there is no conclusion about whether there is phenotypic switching of VSMCs in TAA.Aim:To analyse the phenotypic switching of VSMCs in TAA.Methods:From January 2015 to January 2016,the ascending aorta specimens removed from TAA patients were collected as AA group,and the ascending aorta specimens removed from heart transplantation were collected as no-AA group.Histological changes of the two groups were observed by H&E and Masson.A comparison of the expression levels of SM22α、SMα-actin、OPN in the two samples was made by western blot.Additionally,the phenotypic switching of VSMCs in TAA was detected in rat aneurysm model.Results:H&E and masson showed well-structured,well-colored,clear nucleus of VSMCs,and less collagen deposition in the no-AA group.Conversely,in AA-group,VSMCs lost their original fusiform and typical orderly structures,elastic fibers fracture,collagen deposits obviously.Western blot showed that the expression of SM22α、SMα-actin decreased significantly,while the expression of OPN increased significantly in human TAA tissue.Immunohistochemistryl results showed that the expression of SMα-actin was also significantly reduced in rat TAA tissue.Conclusion:Phenotypic switching of VSMCs does take place in TAA.Background: COMP is a 524-k Da pentamericnon collagenous glycoprotein expressed in all types of cartilage,and its mutation can cause problems of osteogenesis in human beings.COMP,which is identified as a normal component of the artery wall and secreted by VSMCs recently,is necessary for VSMCs to maintain contraction phenotype and contraction function.However,whether COMP is involved in phenotypic switching of VSMCs in aneurysm has not been studied.Aim:To study the expression of COMP in TAA.Methods: From January 2015 to January 2016,the ascending aorta specimens removed from TAA patients were collected as AA groups;and the ascending aorta specimens removed from heart transplantation were collected as no-AA group.A comparison of the expression of COMP,MMP-9 and ADAMTS-7 in the two groups was made by western blot and immunohistochemistry.Meanwhile,the expression of COMP in rat TAA was also analysed.Results: In both human and rat specimens,the expression of COMP decreased significantly in the AA group(p<0.05).The expression of MMP-9,ADAMTS-7 increased significantly(p<0.05)in the human AA group.Conclusion: A decrease in the expression of COMP in TAA,which may be associated with an increase of ADAMTS-7,ADAMTS-7/COMP may be a new therapeutic target for TAA. |
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