Mangrove species and site elevation are critical drivers of greenhouse gas fluxes from restored mangrove soils.

The combined influences of species selection (Avicennia marina, Kandelia obovata) and site elevation (BSL site, below local mean sea level; ASL site, above local mean sea level) on the greenhouse gas fluxes (nitrous oxide (N2O), methane (CH4) and carbon dioxide (CO2)) from restored mangrove soils are investigated in this study. Compared with the A. marina forest, soils in the K. obovata forest at ASL site have higher CO2 fluxes, while higher N2O fluxes in the K. obovata forest are found at BSL site. The highest CH4 fluxes are found at BSL site in the A. marina forest. At each elevation site, the A. marina forest has lower CO2-equivalent fluxes and carbon release in the form of carbon-containing gases. The results suggest that A. marina should be selected for mangrove restoration to minimize carbon release and reduce influence of greenhouse gas fluxes on the global greenhouse effect.

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy.

The mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy.