MiR-195 Promotes Stanford A Acute Aortic Dissection By Regulating Smad7 Expression

ObjectiveBy studying the expression of miR-195 and Smad7 in acute Stanford type A aortic dissection,and the interaction between them,exploring the impact of the relationship of them on the occurrence of acute Stanford A dissection and its clinical significance.Methods12 cases of acute A type aortic dissection who received replacement of ascending aorta and total aortic arch combined with implantation of a stented trunk into the descending aorta were selected as AD group;12 cases of aortic aneurysm underwent Bentall surgery?David surgery or Wheat surgery were selected as AA group;6 cases of coronary heart disease were selected as CAD group.Abandoned tissues of ascending aorta were collected during operations.HE staining and immunohistochemistry staining of TGF-?1 and SMAD7 were performed in paraffin-embedded sections.Western blot was also enrolled to measure the expressions of TGF-?1 and SMAD7 semi-quantitatively.The proliferation of human vascular smooth muscle cells was induced by miR-195,NC,down-regulated miR-195 and NC respectively.After 48 and 48 hours,the growth of the cells was observed under microscope.The expression of miR-195 was detected by q RT-PCR and Wesern Blot was used to detected the expression of TGF-?1 and Smad7 in five groups of cells.ResultsHistological examinations showed significant changes of the media of aortic dissection,as evidenced by the weakness and degeneration of the media,the loose arrangement of elastic fiber and collagen fiber and the inflammatroy infiltration,while a normal media was detected in CAD group.Expressions of TGF-?1 was positive in tissues of AD group and AA group,whereas weak expressions in the CAD group.Smad7 was expressed in all three groups,whereas coronary heart disease group was significantly higher than aneurysm group and dissection group.Western Blotsemi-quantitative analysis showed that the expression of TGF-? in dissection group was significantly higher than that in coronary heart disease group(P <0.05),and Smad7 expression was significantly lower than that in coronary heart disease group(P<0.05).miR-195 was significantly higher in aneurysm group and dissection group than in coronary heart disease group(P <0.05).In in vitro cytology experiments,the expression of TGF-?1 in miR-195-infected human vascular smooth muscle cells was significantly higher than that in the uninfected and mimic NC groups,and the Smad7 expression was significantly lower than that in the uninfected and mimic NC groups.However,after down-regulating miR-195-infected human vascular smooth muscle cells,the expression of TGF-?1 was significantly lower than that of uninfected and mimic NC group cells,and it was significantly lower than that of cells infected with miR-195.Smad7 expression was lower than that of mimic NC and mimic NC.The number of cells in the group was significantly increased,and the number of cells infected with miR-195 was significantly decreased.The above results indicate that the expression of TGF-?1 may be related to miR-195 in human vascular smooth muscle cells,and the specific expression is that miR-195 promotes the expression of TGF-?1.At the same time,miR-195 inhibits the expression of Smad7 and over-expression of Smad7 by down-regulating miR-195.ConclusionsmiR-195 may regulate the occurrence and development of aortic dissection by inhibiting Smad7 expression.