Hui-Bin Liu

Harbin Medical University, Charbin, Heilongjiang Sheng, China

Are you Hui-Bin Liu?

Claim your profile

Publications (7)28.36 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Vascular endothelial cells line the luminal surface of blood vessels, which are exposed constantly to mechanical stimuli, such as fluid shear stress, cyclic strain,and blood pressure. In recent years, more and more evidence indicate that endothelial cells (ECs) sense these mechanical stimuli and subsequently convert mechanical stimuli into intracellular signals. The properties of ECs, that sense the mechanical stimuli, are defined as mechanosensors. There are a variety of mechanosensors have been identified in ECs. These mechanosensors play an important role in regulating function of endothelium and vascular function, including blood pressure. This review focus on the mechanosensors that have been identified in ECs and on what roles mechanosensors play in regulation of endothelium function, as well as in regulation of vascular function.
    Journal of cardiovascular pharmacology 02/2013; · 2.83 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Identifying the key factor mediating pathological cardiac hypertrophy is critically important for developing the strategy to protect against heart failure. Bone morphogenetic protein-4 (BMP4) is a mechanosensitive and proinflammatory gene. In this study, we investigated the role of BMP4 in cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. The in vivo pathological cardiac hypertrophy models were induced by pressure-overload and angiotensin (Ang) II constant infusion in mice, and the in vitro model was induced by Ang II exposure to cultured cardiomyocytes. The expression of BMP4 increased in pressure overload, Ang II constant infusion-induced pathological cardiac hypertrophy, but not in swimming exercise-induced physiological cardiac hypertrophy in mice. BMP4 expression also increased in Ang II-induced cardiomyocyte hypertrophy in vitro. In turn, BMP4 induced cardiomyocyte hypertrophy, apoptosis, and cardiac fibrosis, and these pathological consequences were inhibited by the treatment with BMP4 inhibitors noggin and DMH1. Moreover, Ang II-induced cardiomyocyte hypertrophy was inhibited by BMP4 inhibitors. The underlying mechanism that BMP4-induced cardiomyocyte hypertrophy and apoptosis was through increasing NADPH oxidase 4 expression and reactive oxygen species-dependent pathways. Lentivirus-mediated overexpression of BMP4 recapitulated hypertrophy and apoptosis in cultured cardiomyocytes. BMP4 inhibitor DMH1 inhibited pressure overload-induced cardiac hypertrophy in mice in vivo. The plasma BMP4 level of heart failure patients was increased compared with that of subjects without heart failure. In summary, we conclude that BMP4 is a mediator and novel therapeutic target for pathological cardiac hypertrophy.
    Hypertension 12/2012; · 6.87 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Curcumin is reported to exert antioxidant, anti-inflammatory, antiviral, antibacterial, antifungal, and anti-tumor activities. The human ether-a-go-go related gene (hERG) encodes the rapid component of the delayed rectifier K⁺ currents. Inhibition of hERG K⁺ channels leads to cardiac repolarization prolongation, which contributes to either the anti-arrhythmic effects of anti-arrhythmic drugs, or the pro-arrhythmic effects (induction of long QT syndrome) of some drugs not used for anti-arrhythmias. Since curcumin shows multiple beneficial effects and clinical significance, the aim of the present study is to investigate the effect of curcumin on hERG K⁺ channels, elucidating its potential cardiac therapeutic or toxic effects. In whole-cell patch-clamp experiments, we found that curcumin inhibited hERG K⁺ currents in HEK293 cells stably expressing hERG channels in a dose-dependent manner, with IC₅₀ value of 5.55 μM. The deactivation, inactivation and the recovery time from inactivation of hERG channels were significantly changed by acute treatment of 10 μM curcumin. Incubation of 20 μM curcumin for 24h reduced the HEK293 cell viability. Intravenous injection of maximal amount of curcumin in rabbits (20 mg/animal) did not affect the cardiac repolarization manifested with QTc value. We conclude that curcumin inhibits hERG K⁺ channels in vitro.
    Toxicology Letters 11/2011; 208(2):192-6. · 3.15 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: HIV-infected patients have a high prevalence of long QT syndrome (LQTs). hERG K(+) channel encoded by human ether-a-go-go related gene contributes to IKr K(+) currents responsible for the repolarization of cardiomyocytes. Inhibition of hERG K(+) channels leads to LQTs. HIV Tat protein, the virus transactivator protein, plays a pivotal role in AIDS. The aim of the present study is to examine the effects of HIV Tat protein on hERG K(+) channels stably expressed in HEK293 cells. The hERG K(+) currents were recorded by whole-cell patch-clamp technique and the hERG channel expression was measured by real-time PCR and Western blot techniques. HIV Tat protein at 200 ng/ml concentration showed no acute effect on hERG currents, but HIV Tat protein (200 ng/ml) incubation for 24 h significantly inhibited hERG currents. In HIV Tat incubated cells, the inactivation and the recovery time from inactivation of hERG channels were significantly changed. HIV Tat protein incubation (200 ng/ml) for 24h had no effect on the hERG mRNA expression, but dose-dependently inhibited hERG protein expression. The MTT assay showed that HIV Tat protein at 50 ng/ml and 200 ng/ml had no effect on the cell viability. HIV Tat protein increased reactive oxygen species (ROS) generation and the inhibition of hERG channel protein expression by HIV Tat protein was prevented by antioxidant tempol. HIV Tat protein in vivo treatment reduced IKr currents and prolonged action potential duration of guinea pig cardiomyocytes. We conclude that HIV Tat protein inhibits hERG K(+) currents through the inhibition of hERG protein expression, which might be the potential mechanism of HIV infection induced LQTs.
    Journal of Molecular and Cellular Cardiology 07/2011; 51(5):876-80. · 5.15 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Heme oxygenase-1 (HO-1) shows multiple beneficial effects on cardiovascular diseases. However, the effect of HO-1 on the injury of artery has never been identified. In the present study, we established systemic HO-1 overexpression transgenic mice and investigated the effect of HO-1 on the injury of artery induced by electric stimulation and pressure-overload in transgenic mice. Artery injury was induced by electric stimulation and pressure overload. The contractive function, endothelium-dependent and -independent relaxation of arteries were measured through an isometric force transducer connected to a multichannel acquisition and analysis system. Western blot results showed that HO-1 protein level in transgenic mice arteries was significantly higher than that in wild type mice arteries, while no difference of HO-2 protein level in the arteries of transgenic and wild type mice. Arterial reendothelialization after electric injury was accelerated in transgenic mice. No significant difference in contractive function, endothelium-dependent and -independent relaxation of arteries was observed between wild type and transgenic mice at day 7 after electric injury and 4 weeks after pressure overload. We concluded that HO-1 overexpression accelerated the reendothelialization, but did not prevent the functional impairment of injured artery in mice.
    European journal of pharmacology 03/2011; 659(2-3):199-205. · 2.59 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Heme oxygenase-1(HO-1) has been reported to protect against cardiac hypertrophy in cultured neonatal cardiomyocytes treated with HO-1 inducer, cardiac specific HO-1 transgenic mice, or animals treated with HO-1 inducer. The aim of the present study is to examine the effects of systemic HO-1 transgenic overexpression on pressure overload-induced cardiac hypertrophy in mice. Pressure-overload cardiac hypertrophy was induced by transverse aortic constriction (TAC) in WT (wild type) and systemic HO-1 transgenic overexpression (TG) mice. We found that systemic HO-1 transgenic overexpression aggravated pressure overload-induced cardiac hypertrophy. Pressure-overload induced the more increases of heart weight/ body weigh index, left ventricular weight/ body weight index, β-MHC protein expression, cardiac interstitial fibrosis in TG mice than in WT mice. Pressure-overload increased cardiac HO-1 protein expression in WT but not TG mice, but the cardiac HO-1 protein level was still higher in TAC-treated TG mice than in TAC-treated WT mice. The basal cardiac calcineurin protein level in TG mice was lower than that in WT mice. Pressure-overload increased calcineurin protein expression in both WT and TG mice; however, pressure-overload induced more calcineurin protein expression in TG mice than in WT mice. This study shows for the first time that systemic HO-1 transgenic overexpression aggravates pressure overload-induced cardiac hypertrophy.
    Cellular Physiology and Biochemistry 01/2011; 28(1):25-32. · 3.42 Impact Factor
  • Hui-Bin Liu, Bao-Feng Yang, De-Li Dong
    [Show abstract] [Hide abstract]
    ABSTRACT: Calcineurin is a cytoplasmic Ca(2+)/calmodulin-dependent protein phosphatase that contributes to cardiac hypertrophy. Numerous studies have demonstrated that calcineurin/nuclear factor of activated T cell pathway affects the architecture of the heart under pathologic conditions, and the effects of calcineurin/nuclear factor of activated T cell pathway on cardiac hypertrophy have been well reviewed. Cardiac electrical remodeling is generally accompanied with the cardiac hypertrophy, and alteration of cardiac ion channel activity also leads to the changes of calcineurin activity and cardiac hypertrophy. Many studies have linked calcineurin with changes of a variety of ion channels, but the therapeutic approaches to target calcineurin for correcting cardiac electrical disturbance have not been formulated. Here, we review the recent progress in calcineurin and electrical remodeling in pathologic cardiac hypertrophy.
    Trends in cardiovascular medicine 07/2010; 20(5):148-53. · 4.37 Impact Factor