Effects of miR-29a and miR-101a Expression on Myocardial Interstitial Collagen Generation After Aerobic Exercise in Myocardial-infarcted Rats.

BACKGROUND AND AIMS: Myocardial infarction (MI) is accompanied by increased collagen deposition, cell necrosis and angiogenesis in cardiac tissue, which results in reduced ventricular compliance. Both microRNA-29a (miR-29a) and microRNA-101a (miR-101a) target the mRNAs encoding collagens and other proteins involved in fibrosis. METHODS: We assessed the effects of intermittent aerobic exercise on the expression of cardiac miR-29a and miR-101a and following effects on the TGFß, fos, Smad2/3, COL1A1 and COL3A1 in MI model of rats. Intermittent aerobic exercise for MI rats was begun from the second week and ended at the ninth week postsurgery. Expressions of microRNAs (miRNAs) and fibrosis-associated genes were detected from the infarction adjacent region located in the left ventricle. The heart coefficient (HC = heart weight/body weight) and hemodynamics assay were used to evaluate cardiac function level. RESULTS: Intermittent aerobic exercise inhibited myocardial interstitial collagen deposition and significantly improved cardiac function of MI rats. The results of real-time PCR and Western blot indicate that intermittent aerobic exercise enhanced the expression of miR-29a and miR-101a and inhibited TGFß pathway in the MI rats. CONCLUSIONS: Our results suggest that controlled intermittent aerobic exercise can inhibit TGFß pathway via up-regulation to the expression of miR-29a and miR-101a and finally cause a reduced fibrosis and scar formation in cardiac tissue. We believe that controlled intermittent aerobic exercise is beneficial to the healing and discovery of damaged cardiac tissues and their function after MI.

ANXA2 enhances the progression of hepatocellular carcinoma via remodeling the cell motility associated structures.

Hepatocellular carcinoma (HCC) ranks as the fifth most common malignancy worldwide. The detailed mechanism of signal regulation for HCC progression is still not known, and the high motility of cancer cells is known as a core property for cancer progression maintenance. Annexin A2 (ANXA2), a calcium-dependent phospholipids binding protein is highly expressed in HCC. To study the roles the excessively expressed ANXA2 during the progression of HCC, we inhibited the ANXA2 expression in SMMC-7721 cells using RNAi, followed by the analysis of cell growth, apoptosis and cell motility. To explore the relationship between the cell behaviors and its structures, the microstructure changes were observed under fluorescence microscopy, laser scanning confocal microscopy and electron microscopy. Our findings demonstrated that down-regulation of ANXA2 results in decreased the cell proliferation and motility, enhanced apoptosis, suppressed cell pseudopodia/filopodia, inhibited expression of F-actin and ß-tubulin, and inhibited or depolymerized Lamin B. The cell contact inhibition was also analyzed in the paper. Take together, our results indicate that ANXA2 plays an important role to enhance the malignant behaviors of HCC cells, and the enhancement is closely based on its remodeling to cell structures.