Circ-sh3rf3/GATA-4/miR-29a regulatory axis in fibroblast-myofibroblast differentiation and myocardial fibrosis.

The transdifferentiation from cardiac fibroblasts to myofibroblasts is an important event in the initiation of cardiac fibrosis. However, the underlying mechanism is not fully understood. Circ-sh3rf3 (circular RNA SH3 domain containing Ring Finger 3) is a novel circular RNA which was induced in hypertrophied ventricles by isoproterenol hydrochloride, and our work has established that it is a potential regulator in cardiac hypertrophy, but whether circ-sh3rf3 plays a role in cardiac fibrosis remains unclear, especially in the conversion of cardiac fibroblasts into myofibroblasts. Here, we found that circ-sh3rf3 was down-regulated in isoproterenol-treated rat cardiac fibroblasts and cardiomyocytes as well as during fibroblast differentiation into myofibroblasts. We further confirmed that circ-sh3rf3 could interact with GATA-4 proteins and reduce the expression of GATA-4, which in turn abolishes GATA-4 repression of miR-29a expression and thus up-regulates miR-29a expression, thereby inhibiting fibroblast-myofibroblast differentiation and myocardial fibrosis. Our work has established a novel Circ-sh3rf3/GATA-4/miR-29a regulatory cascade in fibroblast-myofibroblast differentiation and myocardial fibrosis, which provides a new therapeutic target for myocardial fibrosis.

Roles and mechanisms of Ca2+ in regulating primary root growth of plants.

Calcium (Ca2+) as a universal signal molecule plays pivotal roles in plant growth and development. It regulates root morphogenesis mainly through mediating phytohormone and stress signalings or affecting these signalings. In recent years, much progress has been made in understanding the roles of Ca2+ in primary root development. Here, we summarize recent advances in the functions and mechanisms of Ca2+ in modulating primary root growth in plants under normal and stressful conditions.

Responses of soil active carbon and nitrogen to short-term warming in alpine treeline of west Sichuan, China.

Alpine treeline ecosystem is more sensitive to global warming under low temperature limitation with the aggravation of greenhouse effect, which may directly affect plant growth and soil carbon and nitrogen processes. We expected that climate warming would change soil active carbon and nitrogen content in alpine ecosystems. This experiment was conducted in long-term research station of alpine forest ecosystems, in Lixian County, Sichuan Province. The open top camber (OTC) was used to simulate warming, intact soil core (soil organic layer and mineral soil layer) of OTC and CK were collected in April, July and October 2017. Soil dissolved organic carbon (DOC), soil microbial biomass carbon (MBC), dissolved organic nitrogen (DON) and soil microbial biomass nitrogen (MBN) were measured. The results showed that average temperature increased by 0.88 ℃ for air, 0.48 ℃ for soil organic layer and 0.23 ℃ for mineral soil layer. The simulated warming did not significantly change soil organic matter and water content, but significantly increased pH of mine-ral soil layer, and significantly reduced DOC and DON contents of mineral soil layer in non-growing season. There was significant seasonal variation for the contents of DOC, DON and MBN in the two layers, but not for MBC. The MBC and MBN contents of soil organic layer were significantly higher than that of mineral soil layer. There was a significant positive correlation between active carbon and nitrogen with soil organic matter and water content. There was a significant positive correlation between MBC, MBN and soil pH, whereas MBN was negatively correlated with soil temperature.

Real-time monitoring of phenazines excretion in Pseudomonas aeruginosa microbial fuel cell anode using cavity microelectrodes.

Phenazines are a kind of metabolites that can mediate extracellular Pseudomonas aeruginosa (P. aeruginosa) cells in microbial fuel cells (MFCs). However, it is still not clear that whether and how the excretion profile of phenazines is affected by the operating MFC. Here, we report a real time analysis approach based on a cavity microelectrode electrochemical sensor to investigate the phenazines excretion behavior of P. aeruginosa during MFC operation. The phenazine concentration increases at first 72 h, reaches a plateau and decreases after 120 h and also shows local dependent variation. It is dependent on the MFC current generation profile but also affect by the biofilm formation. Accordingly, a mechanism about phenazines excretion in MFC anode and the phenazines mediated extracellular electron transfer of the P. aeruginosa anode is proposed. This work provides a novel strategy for self-mediated extracellular electron transfer analysis in the operating MFCs.

EGF Protects Cells Against Dox-Induced Growth Arrest Through Activating Cyclin D1 Expression.

It has been reported that the antitumor drug doxorubicin (Dox) exerts its toxic effects via GATA-4 depletion and that over-expression of GATA-4 reverses Dox-induced toxicity and apoptosis; however, the precise mechanisms remain unclear. In this study, we observed, for the first time, that EGF protects cells against Dox-mediated growth arrest, G2/M-phase arrest, and apoptosis. Additionally, EGF expression was down-regulated in Dox-treated cells and up-regulated in GATA-4 over-expressing cells. Utilizing real-time PCR and western blotting analysis, we found that the expression of the cell cycle-associated protein cyclin D1 was inhibited in GATA-4-silenced cells and Dox-treated cells and was enhanced in GATA-4 over-expressing cells and EGF-treated cells. Furthermore, EGF treatment reversed the inhibited expression of cyclin D1 that was mediated by GATA-4 RNAi or Dox. Our results indicate that EGF, as a downstream target of Dox, may be involved in Dox-induced toxicity as well as in the protective role of GATA-4 against toxicity induced by Dox via regulating cyclin D1 expression, which elucidates a new molecular mechanism of Dox toxicity with important clinical implications.

EGF is required for cardiac differentiation of P19CL6 cells through interaction with GATA-4 in a time- and dose-dependent manner.

The regulation of cardiac differentiation is critical for maintaining normal cardiac development and function. The precise mechanisms whereby cardiac differentiation is regulated remain uncertain. Here, we have identified a GATA-4 target, EGF, which is essential for cardiogenesis and regulates cardiac differentiation in a dose- and time-dependent manner. Moreover, EGF demonstrates functional interaction with GATA-4 in inducing the cardiac differentiation of P19CL6 cells in a time- and dose-dependent manner. Biochemically, GATA-4 forms a complex with STAT3 to bind to the EGF promoter in response to EGF stimulation and cooperatively activate the EGF promoter. Functionally, the cooperation during EGF activation results in the subsequent activation of cyclin D1 expression, which partly accounts for the lack of additional induction of cardiac differentiation by the GATA-4/STAT3 complex. Thus, we propose a model in which the regulatory cascade of cardiac differentiation involves GATA-4, EGF, and cyclin D1.

Removal of rhodamine B using iron-pillared bentonite.

The iron-pillared bentonite (Fe-Ben) was prepared by ion-exchange using the natural bentonite (GZ-Ben) from Gaozhou, China, at room temperature without calcination. Both Fe-Ben and GZ-Ben were characterized by X-ray diffraction, N(2) adsorption and Fourier transform infrared spectroscopy. The results show that the d(001) value and surface area of the bentonite material increased after iron pillaring. Fe-Ben adsorbed much more Rhodamine B (RhB) than GZ-Ben, which can be ascribed to the special surface properties and large surface area of Fe-Ben. The optimum pH value for the adsorption of RhB on Fe-Ben is 5.0. The adsorption of RhB onto Fe-Ben can be well described by the pseudo-second-order kinetic model and the intraparticle diffusion kinetic model. The adsorption isotherm of RhB onto Fe-Ben matches well with the Langmuir model.

Modeling of alphak/gamma2 (k=1, 2, 3 and 5) interface of GABA A receptor and docking studies with zolpidem: implications for selectivity.

The three-dimensional models of the alphak/gamma2 (k=1, 2, 3 and 5) interface of GABA(A) receptors, which included the agonist-binding site, were constructed and validated by molecular modeling technology. To investigate the mechanism of alpha subunit selectivity of zolpidem, docking calculations were used to illustrate the potential binding modes of zolpidem with different alpha subtypes. The results revealed that there were three reasons resulting in the distinct binding affinity of zolpidem to different alpha subtype. Firstly, the number of hydrogen bonds of agonist-receptor complex would determine the magnitude of binding affinity. Secondly, the His residue in loop A of alpha subunit was indicated as a key role of benzodiazepine binding. Thirdly, the side chain of Glu in loop C reduced the affinity of zolpidem to those receptors containing alpha2, alpha3 or alpha5 subunits.