Key result
Adiponectin-modified bone marrow mesenchymal stem cells significantly improved cardiac function and reduced myocardial fibrosis in diabetic rats by inhibiting the TGF-beta1/Smad signaling pathway.
Why the study?
Bone marrow mesenchymal stem cells have therapeutic potential for diabetes and heart diseases, but their effects on reducing myocardial fibrosis need to be optimized.
Do adiponectin-modified BMSCs alleviate myocardial fibrosis in diabetic rats?
Do adiponectin-modified BMSCs alleviate myocardial fibrosis in diabetic rats?
p-value: p=<0.01
Adiponectin-modified BMSCs may offer a novel therapeutic approach for diabetic cardiomyopathy by reducing cardiac fibrosis via the TGF-beta1/smad pathway.
Hypothesis-generating for modified stem cell therapy in diabetic cardiomyopathy; leaves open clinical translation pending human studies.
Background: Accumulating evidence suggested that bone marrow mesenchymal stem cells (BMSCs) have therapeutic potential for diabetes and heart diseases. However, the effects of BMSC on reducing myocardial fibrosis need to be optimized. This study aimed to investigate the mechanism of adiponectin (APN) modified BMSCs on myocardial fibrosis in diabetic model in vivo and in vitro . Methods: The high-fat diet combined with streptozotocin (STZ) injection were used to induced diabetic rat model. H9c2 cells were cultured under a high glucose medium as in vitro model. The BMSCs were modified by APN plasmid or APN small interfering RNA (siRNA), then transplanted to the diabetic rats by a single tail-vein injection, or co-cultured with H9c2 cells. Results: We demonstrated that diabetic rats showed typical diabetic symptoms, such as decreased cardiac function, accumulation of pathological lesions and collagen expression. However, these impairments were significantly prevented by the APN modified BMSCs treatment while no effects on APN siRNA modified BMSCs treated diabetic rats. Moreover, we confirmed that APN modified BMSCs could attenuate the expression of TGF-beta1/smad to suppress the myocardial fibrosis in the diabetic rats and high glucose induced H9c2 cells. Conclusion: The present results for the first time showed that APN modified BMSCs exerted protection on cardiac fibrosis via inhibiting TGF-beta1/smad signal pathway in diabetic rats. Our findings suggested that APN modified BMSCs might be a novel and optimal therapy for the diabetic cardiomyopathy in future.
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Meng et al. (2021) studied Diabetic cardiomyopathy and myocardial fibrosis (n=60). Adiponectin modified BMSCs vs. Vehicle-modified BMSCs, APN-siRNA modified BMSCs, and untreated diabetic controls was evaluated on Myocardial fibrosis and cardiac function (LVEF, FS) (p=<0.01). Adiponectin-modified bone marrow mesenchymal stem cells significantly improved cardiac function and reduced myocardial fibrosis in diabetic rats by inhibiting the TGF-beta1/Smad signaling pathway.
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