Hsa_circ_0072765 knockdown inhibits proliferation, activation and migration in transforming growth factor-beta (TGF-ß)-induced hepatic stellate cells (HSCs) by the miR-197-3p/TRPV3 axis.

BACKGROUND: Circular RNAs (circRNAs) participate in the progression of diverse human diseases. However, the effects of circRNAs on liver fibrosis are limited. In this study, we aimed to investigate the functions of hsa_circ_0072765 in liver fibrosis. METHODS: Transforming growth factor-beta (TGF-ß)-treated hepatic stellate cells (HSCs) were used as the cell model of liver fibrosis. Quantitative real-time polymerase chain reaction (qRT-PCR) or western blot was performed to determine the expression of hsa_circ_0072765, microRNA-197-3p (miR-197-3p) and transient receptor potential cation channel subfamily V member 3 (TRPV3). 5'-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry analysis and wound-healing assay were conducted to evaluate cell proliferation, cell cycle and migration. HSC activation was assessed by determining the expression of alpha-smooth muscle actin (α-SMA) and type I collagen alpha 1 (Col1A1). Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) were manipulated to analyze the relationship of hsa_circ_0072765, miR-197-3p and TRPV3. The exosome morphology was observed under transmission electron microscopy (TEM). RESULTS: Hsa_circ_0072765 level was increased in TGF-ß-induced HSCs. Hsa_circ_0072765 knockdown inhibited cell proliferation, cell cycle, activation and migration in TGF-ß-induced HSCs. Hsa_circ_0072765 sponged miR-197-3p and negatively regulated miR-197-3p expression. MiR-197-3p inhibition reversed the effects of hsa_circ_0072765 knockdown on TGF-ß-induced HSC proliferation, cell cycle, activation and migration. In addition, TRPV3 was the target gene of miR-197-3p and miR-197-3p overexpression inhibited TGF-ß-treated HSC proliferation, cell cycle, activation and migration by targeting TRPV3. Besides, we found that exosomal hsa_circ_0072765 was increased in TGF-ß-treated HSCs. CONCLUSION: Hsa_circ_0072765 promoted the progression of TGF-ß-treated HSCs by decoying miR-197-3p and upregulating TRPV3.

Chlorine dioxide-iodide-methyl acetoacetate oscillation reaction investigated by UV-vis and online FTIR spectrophotometric method.

In order to study the chemical oscillatory behavior and mechanism of a new chlorine dioxide-iodide ion-methyl acetoacetate reaction system, a series of experiments were done by using UV-Vis and online FTIR spectrophotometric method. The initial concentrations of methyl acetoacetate, chlorine dioxide, potassium iodide, and sulfuric acid and the pH value have great influence on the oscillation observed at wavelength of 289 nm. There is a preoscillatory or induction period, and the amplitude and the number of oscillations are associated with the initial concentration of reactants. The equations for the triiodide ion reaction rate changing with reaction time and the initial concentrations in the oscillation stage were obtained. Oscillation reaction can be accelerated by increasing temperature. The apparent activation energies in terms of the induction period and the oscillation period were 26.02 KJ/mol and 17.65 KJ/mol, respectively. The intermediates were detected by the online FTIR analysis. Based upon the experimental data in this work and in the literature, a plausible reaction mechanism was proposed for the oscillation reaction.

Experimental Study of Closed System in the Chlorine Dioxide-Iodide-Sulfuric Acid Reaction by UV-Vis Spectrophotometric Method.

The mole ratio r(r = [I(-)](0)/[ClO(2)](0)) has great influence on ClO(2)-I(-)-H(2)SO(4) closed reaction system. By changing the initiate concentration of potassium iodide, the curve of absorbance along with the reaction time was obtained at 350 nm and 297 nm for triiodide ion, and 460 nm for iodine. The changing point of the absorbance curve's shape locates at r = 6.00. For the reaction of ClO(2)-I(-) in the absence of H(2)SO(4), the curve of absorbance along with the reaction time can be obtained at 350 nm for triiodide ion, 460 nm for iodine. The mole ratio r is equal to 1.00 is the changing point of the curve's shape no matter at which wavelength to determine the reaction. For the reaction of ClO(2)-I(-)-H(+) in different pH buffer solution, the curve of absorbance along with the reaction time was recorded at 460 nm for iodine. When r is greater than 1.00, the transition point of the curve's shape locates at pH 2.0, which is also the point of producing chlorite or chloride for chlorine dioxide at different pH. When r is less than 1.00, the transition point locates at pH 7.0.

Down-regulation of the human ether-a-go-go-related gene in rat cardiac hypertrophy.

INTRODUCTION: Cardiac hypertrophy is a risk factor for QT prolongation and cardiac sudden death. In this study, the authors examined the expressional regulation on the rat human ether-a-go-go-related gene (HERG), which encodes a structural subunit of the rapid component of the delayed rectifier potassium current (I(Kr)), during myocardial hypertrophy using rat as a model system. METHODS: Cardiac hypertrophy was established in Sprague-Dawley rats by coarctation of the abdominal aorta [left ventricular hypertrophy (LVH) group]. Sham-operated rats were defined as control group (Ctrl group). Hemodynamic, morphologic and histologic parameters were recorded 6 weeks after operation. In addition, the expression of HERG was also determined using a combination of real-time polymerase chain reaction, Western blot and immunohistochemical analyses. RESULTS: Compared with the sham-operated Ctrl group, abdominal aortic coarctation induced LVH in the LVH group, as evidenced by significantly increased ratios of heart weight/left ventricular weight to body weight and enlarged left ventricular myocytes in the histologic sections. The hemodynamic profile revealed significant increases in heart rate and left ventricular end-diastolic pressure, as well as a decrease in the maximal rate of left ventricular pressure fall in the LVH rats, when compared with the Ctrl rats. Electrocardiograms showed prolonged QT and corrected QT intervals. On the molecular level, a significant reduction of HERG, messengerRNA and protein was observed in LVH group, which was inversely correlated with prolonged corrected QT (r = -0.842, P = 0.000). CONCLUSION: The expressional down-regulation of HERG gene may constitute a novel mechanism for QT prolongation during cardiac hypertrophy.