Qi Li

Harbin Medical University, Charbin, Heilongjiang Sheng, China

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Publications (5)20.85 Total impact

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    ABSTRACT: Cardiac T-type Ca(2+) channels are reexpressed in atrial and ventricular myocytes under various pathological conditions such as post-myocardial infarction, hypertrophy, and heart failure, but relatively little is known about the mechanisms. Our previous study found that bone morphogenetic protein-4 (BMP4) was reexpressed in pathological cardiac hypertrophy models and BMP4-mediated cardiomyocyte hypertrophy. We hypothesized that BMP4 could upregulate cardiac T-type Ca(2+) channels in HL-1 atrial myocytes. The T-type Ca(2+) currents were recorded by using the patch-clamp technique, and the expressions of Cav3.1 and Cav3.2 were measured by real-time PCR method in HL-1 cells. BMP4 and Cav3.1 mRNA expressions increased in the left atrium from the pressure overload-induced hypertrophy of mice hearts. BMP4 treatment for 48 h induced increase of Cav3.1 but not Cav3.2 mRNA expression in HL-1 cells, and the increase was inhibited by BMP4 inhibitor noggin. Acute treatment with BMP4 did not affect T-type Ca(2+) currents, but chronic treatment (48 h) significantly increased the amplitude of T-type Ca(2+) currents in HL-1 cells. Chronic treatment with BMP4 induced upregulation of NADPH oxidase-4 (NOX4), increase of reactive oxygen species (ROS) level, and activation of mitogen-activated protein kinase (MAPK)-activated protein kinases c-jun N-terminal kinases (JNK) and p38. BMP4-induced upregulation of Cav3.1 mRNA was inhibited by NADPH oxidase inhibitor apocynin, the radical scavenger tempol, JNK inhibitor SP600125, and p38 inhibitor SB203580. In conclusion, BMP4 induces upregulation of Cav3.1 Ca(2+) channels and T-type Ca(2+) currents in HL-1 atrial myocytes through ROS/MAPK pathways.
    Pflügers Archiv - European Journal of Physiology 02/2014; 466(11). DOI:10.1007/s00424-014-1459-5 · 3.07 Impact Factor
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    ABSTRACT: BACKGROUND: Sentinel surveillance of Keshan disease (KD) is limited by unable to give the prevalence rates and their estimates. This study was to find the national KD prevalence and the estimated patient numbers to provide evidence toward modifying the policy of KD prevention and control. METHOD: Using a probability proportional to population size, randomized, multistage, and cluster sampling, we surveyed 101,127, measured grain selenium levels; and surveyed household income with pre-designed questionnaires. RESULTS: The national prevalence rates of KD, chronic KD and latent KD were 2.21%, 0.50%, and 1.71% respectively. Chronic KD patients are mainly in the provinces where KD had been seriously epidemic. The KD prevalence rate was higher in females (2.20%) than in males (1.98%). These were also higher in older age groups. The cases younger than 30years accounted for 13.6%, indicating the possibility that KD is still occurring. Nationally, the estimated numbers of KD and chronic KD patients are 1,675,500 (95% CI, 1,608,500-1,747,300) and 379,800 (95% CI, 346,700-412,800) respectively. Multiple logistic regression analysis indicated that family income was a significant dependent variable (OR: -0.258, 95% CI: -0.332 to -0.185, p<0.001). More than 2000 chronic KD patients found in the study were treated in 2009-2011. The limitation of this study was that sampling size was determined at national level. CONCLUSION: KD is still a public health issue among the people of the historically severe endemic areas. Selenium supplementation, self-management program for chronic KD patients and translation epidemiology of KD surveillance should be strengthened.
    International journal of cardiology 12/2012; 168(2). DOI:10.1016/j.ijcard.2012.11.046 · 6.18 Impact Factor
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    ABSTRACT: Down-regulation of Kv4.3 K⁺ channels commonly occurs in multiple diseases, but the understanding of the regulation of Kv4.3 K⁺ channels and the role of Kv4.3 K⁺ channels in pathological conditions are limited. HEK (human embryonic kidney)-293T cells are derived from HEK-293 cells which are transformed by expression of the large T-antigen. In the present study, by comparing HEK-293 and HEK-293T cells, we find that HEK-293T cells express more Kv4.3 K⁺ channels and more transcription factor Sp1 (specificity protein 1) than HEK-293 cells. Inhibition of Sp1 with Sp1 decoy oligonucleotide reduces Kv4.3 K⁺ channel expression in HEK-293T cells. Transfection of pN3-Sp1FL vector increases Sp1 protein expression and results in increased Kv4.3 K⁺ expression in HEK-293 cells. Since the ultimate determinant of the phenotype difference between HEK-293 and HEK-293T cells is the large T-antigen, we conclude that the large T-antigen up-regulates Kv4.3 K⁺ channel expression through an increase in Sp1. In both HEK-293 and HEK-293T cells, inhibition of Kv4.3 K⁺ channels with 4-AP (4-aminopyridine) or Kv4.3 small interfering RNA induces cell apoptosis and necrosis, which are completely rescued by the specific CaMKII (calcium/calmodulin-dependent protein kinase II) inhibitor KN-93, suggesting that Kv4.3 K⁺ channels contribute to cell apoptosis and necrosis through CaMKII activation. In summary, we establish: (i) the HEK-293 and HEK-293T cell model for Kv4.3 K⁺ channel study; (ii) that large T-antigen up-regulates Kv4.3 K⁺ channels through increasing Sp1 levels; and (iii) that Kv4.3 K⁺ channels contribute to cell apoptosis and necrosis through activating CaMKII. The present study provides deep insights into the mechanism of the regulation of Kv4.3 K⁺ channels and the role of Kv4.3 K⁺ channels in cell death.
    Biochemical Journal 02/2012; 441(3):859-67. DOI:10.1042/BJ20111604 · 4.78 Impact Factor
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    ABSTRACT: This study explores whether the declining prevalence of Keshan disease is associated with increasing selenium levels in Keshan disease areas in Heilongjiang province. Six counties endemic with Keshan disease and three non-endemic counties were selected as study areas. In each county, two townships and in each township one village were chosen in which to survey ten families about head hair, grain, and soil samples and to obtain demographic information. Selenium was measured with hydride generation-atomic fluorescence spectrometry. In each county endemic with Keshan disease, one of the villages was chosen to investigate the prevalence of the disease. We collected 534 head hair samples, 446 staple food samples, and 180 soil samples. The selenium levels of head hair and corn in the endemic counties were significantly lower than those in non-endemic counties. Family demographic information was homologous except for the composition of staple food. More residents in Keshan disease areas preferred flour and corn. The detection rate for latent Keshan disease had a significantly negative correlation with the corn selenium level in six counties endemic with Keshan disease. As the population in this region is still at risk for Keshan disease, selenium surveillance measures should be intensified.
    Biological trace element research 12/2011; 143(3):1255-63. DOI:10.1007/s12011-011-8961-9 · 1.61 Impact Factor
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    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. DOI:10.1016/j.yjmcc.2011.07.017 · 5.22 Impact Factor