Angiotensin II type i receptor agonistic autoantibodies induces apoptosis of cardiomyocytes by downregulating miR21 in preeclampsia: a mechanism study.

The objective of the present study was to explore whether AT1-AA induced cardiomyocyte apoptosis was related to its inhibitory of miR-21 expression. In vivo studies, the pregnant rats were divided into two groups: Sham group, Model group. The pathology, cell apoptosis, and relative protein expressions were evaluated by hematoxylin and eosin staining, and Western blot assay. The expression of microRNA was detected by gene microarray. In the cell experiment, the neonatal rat cardiomyocytes were divided into four groups: NC group, AT1-AA group, and miR-21 group and AT1-AA+miR-21 group. The cell apoptosis and relative proteins' expressions were measured by flow cytometry and Western blot assay. Results: Compared with the Sham group, miR-21 in the cardiac tissue of the model group was downregulated significantly; the expression of p-JNK, Bax and caspases-3 was increased, the expression of Bcl-2 was decreased, and the Bcl-2/Bax ratio became smaller. The expression of miR-21 in AT1-AA treated cardiomyocytes was only 52% of the control group, with an apoptosis rate of 32.6%. In addition, the expression of pPTEN, pAKT and pFOXO3a in the model group was significantly higher than that in the NC group. The cardiomyocyte apoptosis rate in miR-21 overexpression group was only 23.7%, which was higher than that in the NC group, but significantly lower than that in AT1-AA group. PTEN, AKT and FOXO3a phosporylation in miR-21 overexpression group was also lower than that in AT1-AA group. AT1-AA...
Source: American Journal of Translational Research - Category: Research Tags: Am J Transl Res Source Type: research