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Human Umbilical Cord Mesenchymal Stem Cells Alleviate Myocardial Endothelial-Mesenchymal Transition in a Rat Dilated Cardiomyopathy Model

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机构: [a]Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China [b]Department of Neurology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China [c]Department of Pediatrics, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China [d]Department of Paediatrics, Children’s Hospital of Shenzhen, Guangdong, China [e]Department of Pediatrics, Beijing Children’s Hospital, Capital Medical Hospital, Beijing, China [f]Department of Pediatrics, Maternal and Child Health Care Hospital of Pingshan District, Shenzhen, Guangdong, China
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Background. Human umbilical cord derived mesenchymal stem cells (HuMSCs) have been shown to suppress cardiac fibrosis; however, the underlying mechanisms are not fully understood. Recent studies have shown that endothelial-mesenchymal transition (EndMT) plays a crucial part in myocardial fibrosis. In the present study, we investigated the suppressive role of HuMSCs in cardiac fibrosis and related mechanisms in a rat dilated cardiomyopathy (DCM) model. Methods. Male Lewis rats were randomly divided into 3 groups. Rats without any treatment served as a negative control group, while the DCM rats, which were generated by immunization with porcine myosin, were divided into 2 groups: a HuMSC group, in which HuMSCs (1 x 10(6) cells/rat) were injected intravenously, and a vehicle group, in which rats were injected with volume-matched solution containing no HuMSCs. Histologic and immunofluorescent measurements were used to evaluate the effects of HuMSCs on cardiac fibrosis and EndMT. Results. We observed a significant increase in myocardial fibrosis, and elevated EndMT in rats of the vehicle group were observed compared with those in the negative control group along with the increased activity of transforming growth factor (TGF)-beta 1/extracellular signal-regulated kinase (ERK) 1/2 signaling. Treatment with HuMSCs repressed the increase in myocardial fibrosis and EndMT observed in DCM rats, which correlated with decreased activity of TGF-beta 1/ERK1/2 signaling. Conclusion. The HuMSCs attenuated cardiac fibrosis at least partly through the inhibition of TGF-beta 1/ERK-induced EndMT.

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出版当年[2018]版:
大类 | 4 区 医学
小类 | 4 区 免疫学 4 区 外科 4 区 移植
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 免疫学 4 区 外科 4 区 移植
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出版当年[2017]版:
Q4 TRANSPLANTATION Q4 SURGERY Q4 IMMUNOLOGY
最新[2023]版:
Q4 SURGERY Q4 TRANSPLANTATION Q4 IMMUNOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

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第一作者机构: [a]Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China
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通讯机构: [c]Department of Pediatrics, Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China [d]Department of Paediatrics, Children’s Hospital of Shenzhen, Guangdong, China [e]Department of Pediatrics, Beijing Children’s Hospital, Capital Medical Hospital, Beijing, China [f]Department of Pediatrics, Maternal and Child Health Care Hospital of Pingshan District, Shenzhen, Guangdong, China [*1]Department of Paediatrics, Children’s Hospital of Shenzhen, Yi tian Road, Fu Tian, Shenzhen, Guangdong 518000, P.R. China. [*2]Department of Paediatrics, Beijing Children’s Hospital, Capital Medical Hospital, Yue tan Road, Xi Cheng, Beijing, 100032, P.R. China.
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