Pu Dong New Area Peoples Hospital

Shanghai, China

Pu Dong New Area Peoples Hospital

Shanghai, China

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Zhi C.,Pu Dong New Area Peoples Hospital | Huang Y.,Pu Dong New Area Peoples Hospital | Qi W.,Pu Dong New Area Peoples Hospital | Shen J.,Pu Dong New Area Peoples Hospital | And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: To establish obese rat models by high-fat diet, screen microRNAs by microarray in the omental adipose tissue, and find out differential expression of microRNAs in obese rats, for further understanding the role of microRNAs as regulating molecules in obesity-induced lipid metabolism disorders. Methods: 40 male SD rats were randomly divided into normal diet group and high-fat diet group, respectively. After fed for 8 weeks, rats were weighted, measured length and other characteristics were observed. Eye blood was taken to test blood glucose level, blood lipids level, insulin level and other indicators. The omental adipose tissue was measured by electronic analytical scales and saved at-80°C liquid nitrogen. Fat cells were stained by oil red to observe their morphology under microscopy. The expression of microRNAs was screened by microarray, and verified by Real-Time PCR. Results: After high-fat diet for 4 and 8 weeks, some fatty indicators changed, including increased body weight, omental fat weight, triglycerides, total cholesterol, low-density lipoprotein, blood glucose level and insulin level, and decreased high-density lipoprotein, and differential phenotype of fat cells. Besides, by microarray techniques and Real-Time PCR, 13 differential expression microRNAs were identified, including 7 up-regulated microRNAs (microRNA30a, microRNA7e, microRNA30c, microRNA335, microRNA103, microRNA107, microRNA139-5p), and 6 down-regulated microRNAs (microRNA494, microRNA140, microRNA342-5p, microRNA382, microRNA17-1-3p, microRNA92a). Conclusion: Changes in the expression of microRNAs contribute to the pathogenesis of many diseases, including obesity disorders. These alterations can be due to various mechanisms, such as cell proliferation, apoptosis, migration, and differentiation, providing new therapies for diseases. © 2015 E-Century Publishing Corporation. All rights reserved.


Huang Y.,Pu Dong New Area Peoples Hospital | Qi Y.,Pu Dong New Area Peoples Hospital | Du J.-Q.,Pu Dong New Area Peoples Hospital | Zhang D.-F.,Pu Dong New Area Peoples Hospital
Expert Opinion on Therapeutic Targets | Year: 2014

Background: Although few microRNAs (miRNAs) have been involved in the regulation of post-ischemic cardiac fibrosis, the exact effect and underlying mechanism of miRNAs in cardiac fibrosis remains unclear. Here, we sought to investigate whether microRNA-34 (miR-34) plays a role in the pathogenic development of myocardial fibrosis.Methods: The myocardial infarction (MI) mice model was induced and cardiac fibroblasts were cultured. Histological analyses, quantitative real-time polymerase chain reaction and Western blotting analysis were used.Results: We found that the miR-34 cluster, especially miR-34a, was upregulated in the MI heart. In vivo, inhibition of miR-34a reduces the severity of experimental cardiac fibrosis in mice. TGF-β1 increased miR-34a expression in cardiac fibroblasts. Overexpressing miR-34a levels increased the profibrogenic activity of TGF-β1 in cardiac fibroblast, whereas inhibition miR-34a levels weakened the activity. Finally, we showed that miR-34a's underlying mechanism during cardiac fibrosis occurs through the targeting of Smad4 expression.Conclusions: Our findings provide evidence that miR-34a plays a critical role in the progression of cardiac tissue fibrosis by directly targeting Smad4, which suggests that miR-34a may be new marker for cardiac fibrosis progression and that inhibition of miR-34a may be a promising strategy in the treatment of cardiac fibrosis. © 2014 Informa UK, Ltd.


PubMed | Pu Dong New Area Peoples Hospital
Type: Journal Article | Journal: Expert opinion on therapeutic targets | Year: 2014

Although few microRNAs (miRNAs) have been involved in the regulation of post-ischemic cardiac fibrosis, the exact effect and underlying mechanism of miRNAs in cardiac fibrosis remains unclear. Here, we sought to investigate whether microRNA-34 (miR-34) plays a role in the pathogenic development of myocardial fibrosis.The myocardial infarction (MI) mice model was induced and cardiac fibroblasts were cultured. Histological analyses, quantitative real-time polymerase chain reaction and Western blotting analysis were used.We found that the miR-34 cluster, especially miR-34a, was upregulated in the MI heart. In vivo, inhibition of miR-34a reduces the severity of experimental cardiac fibrosis in mice. TGF-1 increased miR-34a expression in cardiac fibroblasts. Overexpressing miR-34a levels increased the profibrogenic activity of TGF-1 in cardiac fibroblast, whereas inhibition miR-34a levels weakened the activity. Finally, we showed that miR-34as underlying mechanism during cardiac fibrosis occurs through the targeting of Smad4 expression.Our findings provide evidence that miR-34a plays a critical role in the progression of cardiac tissue fibrosis by directly targeting Smad4, which suggests that miR-34a may be new marker for cardiac fibrosis progression and that inhibition of miR-34a may be a promising strategy in the treatment of cardiac fibrosis.

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