[MiR-222-3р Regulates the Proliferation and Differentiation of C2C12 Myoblasts by Targeting BTG2].

MiR-222-3р has been implicated in tumor cell proliferation and has an important role in the differentiation and maturation of myogenic cells. However, its role in skeletal myoblast proliferation is still unclear. In this study, we found that miR-222-3р expression increases initially and then decreases during C2C12 myoblast proliferation. Using synthetic miRNA mimics and inhibitors in gain- or loss-of-function experiments, we snowed that miR-222-3р overexpression in C2C12 cells promotes myoblast proliferation and represses myofiber formation, while miR-222-3р downregulation has the opposite effect. Using a prediction program, BTG2 was identified as a possible target gene of miR-222-3р. During myogenesis, miR-222-3р mimics repress BTG2 expression, while miR-222-3р inhibitors promote BTG2 expression. Using dual-luciferase reporter assay, we further demonstrated that miR-222-3р specifically targets BTG2. Additionally, we show that siRNA-mediated downregulation of BTG2 expression in C2C12 myoblasts promotes the proliferation and suppresses differentiation. In conclusion, we provide a novel insight into the mechanism by which miR-222-3р regulates the proliferation and differentiation of C2C12 myoblasts by targeting BTG2. This information contributes to our understanding of the role of miRNAs in skeletal muscle development.

Meta-analysis of the long term effects of different interventions on chronic total coronary occlusions.

BACKGROUND: Coronary chronic total occlusion (CTO) is the end stage of coronary artery atherosclerosis. CTO revascularization can be performed by percutaneous transluminal coronary angioplasty (PTCA), bare metal stent (BMS) or drug-eluting stent (DES). It is important to scientifically evaluate the effectiveness of CTO interventional treatments. METHODS: Relevant studies of long term outcomes for several kinds of CTO treatments were examined. Data were extracted and assessed by two independent clinical experts, pooled and analyzed using meta-analysis. RESULTS: (1) Totally 8 articles comparing outcomes between PTCA and BMS treatment were analyzed. Follow-up variables such as mortality, subsequent coronary artery bypass graft surgery (CABG), re-occlusion, re-stenosis and target lesion revascularization (TLR) were analyzed by meta-analysis. Compared with BMS intervention, PTCA was associated with significant higher rate of re-occlusion, re-stenosis, subsequent PTCA and TLR. (2) Totally 12 articles compared long term outcomes between BMS groups and DES groups, encompassed 3605 CTO patients. During the long-term follow-up, six variables as major adverse cardiac events (MACE), myocardial infarction, all-cause death, subsequent CABG, accumulated MACE-free survival rate, re-stenosis/re-occlusion rate were analyzed by meta-analysis. Compared with patients in DES groups, patients in BMS groups had significant higher MACE, subsequent CABG, re-stenosis/re-occlusion rate, TLR, target vessel revascularization, while lower MACE-free survival rate. CONCLUSIONS: Incidence of re-occlusion, re-stenosis, subsequent PTCA and TLR were significantly lower for BMS implantation than for PTCA procedure. Variables, including MACE, subsequent CABG, re-stenosis/re-occlusion rate were higher while accumulated MACE-free survival rate was lower in BMS groups than in DES groups.

Effect of dexamethasone on cardiovascular response induced by norepinephrine in nucleus tractus solitarii.

AIM: To study the effect of dexamethasone on cardiovascular response induced by norepinephrine (NE) in nucleus tractus solitarii (NTS). METHODS: The variations of cardiovascular action caused by these drugs were observed after injection of mifepristone (Mif), dexamethasone (Dex), bicuculline (Bic), and NE into the medial and intermediate NTS. RESULTS: Microinjection of Dex (0.39 mmol.L-1, 0.1 microL) into the medial and intermediate NTS abolished the vasodepressed response to NE (8 mmol.L-1, 0.1 microL) microinjected into the same area 10 min later, and the inhibition did not disappear until 4 h. The rapid inhibitory effects of Dex on NE vasodepression was not antagonized by Mif (4.66 mumol.L-1, 0.1 microL), but it was blocked by Bic (3.24 mumol.L-1, 0.1 microL). CONCLUSION: Dex abolished cardiovascular response to NE microinjected into NTS which may be mediated by GABAA receptor.