1.Effect of circRNA_000203 on fibrotic phenotypes in mouse cardiac fibro-blasts
Wensi ZHU ; Chunmei TANG ; Jiening ZHU ; Qiuxiong LIN ; Yongheng FU ; Chunyu DENG ; Hui YANG ; Fang RAO ; Shulin WU ; Zhixin SHAN
Chinese Journal of Pathophysiology 2016;32(8):1351-1356
AIM:To determine circular RNA (circRNA) profiles in the diabetic mouse myocardium , and to investigate the effect of circRNA_000203 on fibrotic phenotypes in cardiac fibroblasts .METHODS:Masson trichrome stai-ning was performed on the myocardium of the diabetic db /db mice and the non diabetic db/m control mice .circRNA ex-pression profile in the diabetic myocardium was detected by circRNAs microarray .The expression of circRNA_000203 was determined by real time fluorescence quantitative PCR ( RT-qPCR ) .Recombinant circRNA_000203 adenovirus was pre-pared for enforced the expression of circRNA_000203 in mouse cardiac fibroblasts.The expression of Col1a2, Col3a1andα-SMA was determined in circRNA_000203-modified cardiac fibroblasts , respectively .RESULTS:Masson trichrome stai-ning showed that fibrosis was increased in the diabetic mouse myocardium .The results of circRNA array detection revealed that circRNAs were dysregulated in the diabetic myocardium .circRNA_000203 was up-regulated in the diabetic myocardi-um.Significant over-expression of circRNA_000203 was achieved in the cardiac fibroblasts after infection with the recombi-nant circRNA_000203 adenovirus.The mRNA and protein expression of Col1a2, Col3a1 and α-SMA was significantly in-creased in the cardiac fibroblasts with over-expression of circRNA_000203.CONCLUSION:circRNA_000203 is up-regu-lated in the diabetic mouse myocardium .It has pro-fibrotic effect on the cardiac fibroblasts .
2.MEF2C mediates inhibitory effect of microRNA-214 on cardiomyocyte hypertrophy
Chunmei TANG ; Jiening ZHU ; Wensi ZHU ; Qiuxiong LIN ; Zhiqin HU ; Yongheng FU ; Mengzhen ZHANG ; Chunyu DENG ; Honghong TAN ; Shulin WU ; Zhixin SHAN
Chinese Journal of Pathophysiology 2016;32(8):1345-1350
AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .
3.Quality Evaluation of the Literatures about Medical Insurance Budget Impact Analysis in China and the United States
Pengcheng LIU ; Jiahui GU ; Mingyu BAI ; Yaqi DONG ; Jia’er LIN ; Xihan LIN ; Wensi WU ; Nan PENG ; Rong SHAO ; Wenbing YAO
China Pharmacy 2019;30(12):1684-1691
OBJECTIVE: To provide experience and reference for the study of medical insurance budget impact analysis (BIA) in China. METHODS: Retrieved from PubMed, ProQuest, CNKI, Wanfang database and CBM, related literatures about medical insurance BIA research in China and the United States were collected since the establishment of the database. The basic information, analysis results and data sources were summarized and sorted out, and descriptive analysis of the included literature was carried out on basis of seven key elements such as model design, research perspective, treatment cost, reference scenario, target population, research time limit and discount/inflation, sensitivity analysis. RESULTS: A total of 72 literatures were included in this study, involving 24 (33.33%) studies in China, 48 (66.67%) studies in the United States; the indications of 45 studies were chronic diseases (62.50%), and those of 21 studies were acute diseases (37.50%). Among the research methods, 49 studies (68.06%) used BIA alone and 23 studies (31.94%) adopted BIA combined with pharmaceutical economics. In terms of model design, 50 studies (69.44%) adopted cost calculation models. In terms of research perspective, 60 studies (81.94%) were based on the perspective of medical insurance department research. In the calculation of treatment cost, 69 studies (95.84%) included drug cost. In terms of reference scenarios, 61 studies (84.72%) compared the economics of different drug-based treatment groups. For target population, only 31 (43.06%) studies used real world data. In terms of research duration and discount/inflation, 14 studies (19.44%) used treatment or length of hospitalization to indicate research duration, and 19 studies (26.39%) used discount rate or inflation rate to adjust costs. As for sensitivity analysis, 62 studies (86.11%) conducted sensitivity analysis, of which 49 (68.06%) used single factor sensitivity analysis. CONCLUSIONS: There are still some limitations in medical insurance BIA research literature in China and the United States, such as unreasonable use of data, incomplete coverage of the cost, and unreasonable setting of sensitivity analysis variables. It is recommended that BIA research should standardize data sources to improve the quality of budget evidence quality, reasonably evaluate market size to improve the authenticity of prediction, scientifically set variables and their scope of change to improve the stability of results, establish BIA research paradigms or evaluating standards so as to guide BIA research scientifically.