The expression of Nesprin-1 increased in aortic dissection: why?

BACKGROUND: To detect the expression of Nesprin-1 in aortic dissection (AD) in patients and to investigate the role of Nesprin-1 in the pathogenesis of AD in a mouse model. METHODS: Blood and tissue specimens from AD patients were collected. The expression of Nesprin-1 in tissues from AD patients and non-AD patients with heart disease was studied by western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). In addition, the expression and distribution of Nesprin-1 in AD and sham mice were compared in an induced AD mouse model, and detected by immunohistochemistry and qRT-PCR. RESULTS: Immunoblotting and qRT-PCR both showed that the expression of Nesprin-1 was significantly higher in AD versus control patients. An animal model of AD was established by continuous injection of Ang II into ApoE-/- mice. The expression of Nesprin-1 in aortic tissue of AD mice was higher than that of sham-operated mice as determined by immunohistochemistry. qRT-PCR showed that Nesprin-1 gene expression in aorta of AD mice was higher than that of sham-operated mice. CONCLUSIONS: An increased expression of Nesprin-1 was associated with AD, and hence Nesprin-1 may be involved in the pathogenesis of ADs. Preliminary findings suggest that Nesprin-1 may be a therapeutic target for the treatment of AD.

Mesenchymal stem cells were affected by up-regulation of miRNA-21 in vitro.

BACKGROUND: The expression of miRNA-21 was high in cells that were derived from MSCs, but, the role of miRNA-21in the MSCs was unknown. MATERIAL/METHODS: In this study, flow cytometry, which was used to identify the surface-associated antigens of MSCs. The 10 µmol/l 5-azacytidine was used to induce MSCs to differentiate to cardiomyocyte-like cells. Immunofluorescence, that was for detected the expression of troponin I (cTnI). The samples were assigned to 3 groups: the blank group, the miRNA-21 mimic group, and the negative control (NC) group. The proliferation of MSCs was detected by methyl thiazolylte-trazolium (MTT), the apoptosis of MSCs was analyzed by flow cytometry, Western-blot, which was used to identify the expression of cTNI and myoD in the MSCs. RESULTS: The proliferation of MSCs was increased, because of the over expression of miRNA-21; But, the apoptotic rate of the MSCs were slower in MIRNA-21 group, on account of the expression of miRNA-21 was higher than that of in the NC and CK groups. The expression of cTNI in miRNA-21 group was higher than that of in the NC and CK groups. CONCLUSIONS: The results also suggested that, the up-regulation of miRNA-21 enhanced proliferation of MSCs, reducing the apoptosis of MSCs. MiRNA-21 promotes the differentiation of MSCs, which may pave the way for the treatment directed toward restoring miRNA-21 function for myocardial ischemia.