In the present study, we aimed to investigate the effect of transplantation of cardiac stem cells (CSCs) overexpressing integrin-linked kinase (ILK) on cardiac function of rats with acute myocardial infarction (MI). A total of 60 rats were randomly divided into normal saline (NS) group (n=20), green fluorescent protein (GFP)-CSC group (n=20) and ILK-CSC group (n=20). In the ILK-CSC group, CSCs in rats were transfected with GFP adenovirus vector overexpressing ILK. The rat model of MI was established. The cardiac function 4 weeks after transplantation was detected via echocardiography, and the exhaustive swimming experiment was performed to observe the exercise load capacity. Moreover, Ki-67 and P-H3 proteins in myocardial tissues of rats were detected via immunohistochemistry, and the expression of GFP was observed under a fluorescence microscope. Cells in the GFP-CSC group were transfected with the empty GFP adenovirus, while those in NS group were not transfected, and other treatments in these two groups were the same as those in the ILK-CSC group. Four weeks after transplantation, left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) of rats in the ILK-CSC group were smaller than those in the GFP-CSC group, but left ventricular ejection fraction (LVEF) (69.88±5.61 mm) was higher than that in the GFP-CSC group (P<0.05). The exercise time in the ILK-CSC group (12.69±0.58 min) was longer than that in the GFP-CSC and NS groups (P<0.05). The expression levels of Ki-67 and P-H3 proteins in myocardial cells of rats in the ILK-CSC group were higher than those in the GFP-CSC and NS groups (P<0.05). The number of transplanted cells retained around the infarct region in the ILK-CSC group 3 days after transplantation was obviously larger than that in the GFP-CSC group (P<0.001). Intramyocardial injection of CSCs overexpressing ILK immediately after the establishment of rat model of MI can promote myocardial cell proliferation, improve cardiac function and increase exercise capacity of rats.
Objective: The aim of this study was to explore the role of has_circ_0010452 in the progression of osteoporosis (OP) targeting miR-543, as well as their functions in regulating proliferation and osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs). Methods: The expression levels of circ_0010452 and miR-543 in hBMSCs at different time points of osteogenic differentiation were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). After transfection of circ_0010452 siRNA or miR-543 inhibitor in hBMSCs, the relative expression levels of osteogenic marker proteins, including oat spelt xylan (OSX), osteocalcin (OCN) and collagen I (Col-1), were determined by western blot. Cell proliferation of hBMSCs was valued by Cell Counting Kit 8 (CCK-8) assay. Dual-Luciferase reporter gene assay was performed to verify the relationship between circ_0010452 and miR-543. Subsequently, the regulatory effects of circ_0010452 and miR-543 on osteogenic differentiation and the capability of mineralization were evaluated by alkaline phosphatase (ALP) determination and alizarin red staining, respectively. Results: The expression of circ_0010452 decreased gradually and miR-543 increased in hBMSCs with the prolongation of osteogenic differentiation. circ_0010452 could bind to miR-543, which was negatively regulated by miR-543 in hBMSCs. Moreover, knockdown of circ_0010452 inhibited proliferation and osteogenic differentiation by upregulating miR-543, as well as upregulating expressions of OSX, OCN and Col-1. Furthermore, knockdown of circ_0010452 markedly promoted the capability of mineralization of hBMSCs, which was further reversed by transfection of miR-543 inhibitor. The knockdown of miR-543 partially reversed the inhibitory effect of circ_0010452 on the osteogenesis of hBMSCs. Conclusions: Silence of circ_0010452 promotes the development of OP via binding to miR-543 regulating proliferation and osteogenic differentiation of hBMSCs, thus promoting the progression of osteoporosis.
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