Yihan Chen

Publications (6)20.27 Total impact

• Article: [A novel GATA4 mutation leading to congenital ventricular septal defect].

  Yi-qing Yang, Yong-qing Tang, Xing-yuan Liu, Xiao-ping Lin, Yi-han Chen
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  ABSTRACT: To identify the GATA4 gene mutation of congenital ventricular septal defect (VSD) and study the molecular mechanism of a novel mutation. The clinical data and blood samples from 185 unrelated subjects with congenital VSD were collected and evaluated together with 200 healthy individuals. The coding exons and the flanking intron regions of the GATA4 gene were amplified by PCR and sequenced using the di-deoxynucleotide chain termination approach. The GATA4 gene was cloned and the corresponding mutant was acquired by site directed mutagenesis. The recombinant plasmid expressing GATA4 and the reporter vector expressing enhanced green fluorescence protein (EGFP) driven by the promoter of atrial natrium peptide (ANP) gene were transfected into HeLa cells with Lipofectamine. The effect of mutated GATA4 gene on the transcriptional activity of encoded transcriptional factor was analyzed by reverse transcription (RT)-PCR. A novel heterozygous missense GATA4 mutation, c.191G>A was identified in 1 VSD patient. The mutation leads to glycine to glutamic acid change at amino acid residue 64 (G64E) in the GATA4 protein. Functional analysis showed that GATA4 G64E mutation decreased the transcriptional activity of GATA4 transcriptional factor. A novel heterozygous missense GATA4 mutation, G64E, was identified in 1 VSD patient. The mutation might cause VSD by impairing the transcriptional activity of GATA4 transcriptional factor.
  Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 10/2010; 27(5):512-6.
• Article: Effects of potassium channel blockers on changes in refractoriness of atrial cardiomyocytes induced by stretch.

  Jie Qi, Junjie Xiao, Yangyang Zhang, Jun Li, Ying Liu, Pengjuan Li, Lei Liang, Bing Jiang, Wei Wen, Cuimei Zhao, Dandan Liang, Yi Liu, Yi-Han Chen
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  ABSTRACT: Shortening of the effective refractory period (ERP) is regarded as one of the key mechanisms of atrial fibrillation (AF). Stretch is an important predisposing factor in the pathogenesis of AF. However, effective methods to counteract alteration of ERP induced by stretch still need to be explored. Although potassium channels play important roles in cardiac repolarization and refractoriness, the effects of potassium channel blockers on the alteration of repolarization and refractoriness induced by stretch are still unknown. Action potential duration (APD) and ERP were recorded using the standard intracellular microelectrode technique in the left atrial appendage cardiomyocytes of guinea pigs. Stretch accelerated repolarization of atrial cardiomyocytes and also shortened the ERP (P < 0.05). Dofetilide, a rapid delayed rectifying potassium ion channel (I(Kr)) blocker; 4-AP, a transient outward potassium ion channel (I(to)) blocker; and BaCl(2), an inward rectifying potassium ion channel (I(K1)) blocker could counteract the shortening of APD and ERP (P < 0.01). Glibenclamide, an ATP-sensitive potassium ion channel (I(KATP)) blocker; 293-B, a slow delayed rectifying potassium channel (I(Ks)) blocker; and DPO-1, an ultra-rapid delayed rectifying potassium ion channel (I(Kur)) blocker all had no effect on APD and ERP (P > 0.05). Stretch could accelerate repolarization of atrial cardiomyocytes and shorten their ERP, and the I(to), I(Kr), and I(K1) blockers could counteract the effects of stretch.
  Experimental Biology and Medicine 06/2009; 234(7):779-84. · 2.64 Impact Factor
• Article: Stretch-induced alterations of human Kir2.1 channel currents.

  Yusong He, Junjie Xiao, Yiqing Yang, Qinshu Zhou, Zhimin Zhang, Qin Pan, Yi Liu, Yihan Chen
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  ABSTRACT: The inward rectifier potassium channel, Kir2.1, contributes to the I(K1) current in cardiac myocytes and is closely associated with atrial fibrillation. Strong evidences have shown that atrial dilatation or stretch may result in atrial fibrillation. However, the role of Kir2.1 channels in the stretch-mediated atrial fibrillation is not clear. In this study, we constructed the recombinant plasmid of KCNJ2 that encodes the Kir2.1 channel and expressed it in CHO-K1 cells. We recorded I(K1) currents using the whole-cell patch clamping technique. Our data showed that I(K1) currents were significantly larger under stretch in the hypotonic solution than under non-stretch in the iso-osmotic solution, and the activation kinetics of the Kir2.1 channel were changed markedly by stretch as well. Thus, atrial stretch in human heart might result in excessive I(K1) currents, which is likely to increase the resting membrane potential and decrease the effective refractory period, to initiate and/or maintain atrial fibrillation.
  Biochemical and Biophysical Research Communications 01/2007; 351(2):462-7. · 2.48 Impact Factor
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  Article: A Kir2.1 gain-of-function mutation underlies familial atrial fibrillation.

  Min Xia, Qingfeng Jin, Saïd Bendahhou, Yusong He, Marie-Madeleine Larroque, Yiping Chen, Qinshu Zhou, Yiqing Yang, Yi Liu, Ban Liu, [......], Li Li, Xiongjian Dong, Zhiwen Pan, Rongrong Wang, Haiying Wan, Weiqin Qiu, Wenyuan Xu, Petra Eurlings, Jacques Barhanin, Yihan Chen
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  ABSTRACT: The inward rectifier K(+) channel Kir2.1 mediates the potassium I(K1) current in the heart. It is encoded by KCNJ2 gene that has been linked to Andersen's syndrome. Recently, strong evidences showed that Kir2.1 channels were associated with mouse atrial fibrillation (AF), therefore we hypothesized that KCNJ2 was associated with familial AF. Thirty Chinese AF kindreds were evaluated for mutations in KCNJ2 gene. A valine-to-isoleucine mutation at position 93 (V93I) of Kir2.1 was found in all affected members in one kindred. This valine and its flanking sequence is highly conserved in Kir2.1 proteins among different species. Functional analysis of the V93I mutant demonstrated a gain-of-function consequence on the Kir2.1 current. This effect is opposed to the loss-of-function effect of previously reported mutations in Andersen's syndrome. Kir2.1 V93I mutation may play a role in initiating and/or maintaining AF by increasing the activity of the inward rectifier K(+) channel.
  Biochemical and Biophysical Research Communications 08/2005; 332(4):1012-9. · 2.48 Impact Factor
• Article: Identification of a KCNE2 gain-of-function mutation in patients with familial atrial fibrillation.

  Yiqing Yang, Min Xia, Qingfeng Jin, Saïd Bendahhou, Jingyi Shi, Yiping Chen, Bo Liang, Jie Lin, Yi Liu, Ban Liu, [......], Ning Ma, Xiaoyan Su, Kaiya Niu, Yan Pei, Wenyuan Xu, Zhaopeng Chen, Haiying Wan, Jianmin Cui, Jacques Barhanin, Yihan Chen
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  ABSTRACT: Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice. We first reported an S140G mutation of KCNQ1, an alpha subunit of potassium channels, in one Chinese kindred with AF. However, the molecular defects and cellular mechanisms in most patients with AF remain to be identified. We evaluated 28 unrelated Chinese kindreds with AF and sequenced eight genes of potassium channels (KCNQ1, HERG, KCNE1, KCNE2, KCNE3, KCNE4, KCNE5, and KCNJ2). An arginine-to-cysteine mutation at position 27 (R27C) of KCNE2, the beta subunit of the KCNQ1-KCNE2 channel responsible for a background potassium current, was found in 2 of the 28 probands. The mutation was present in all affected members in the two kindreds and was absent in 462 healthy unrelated Chinese subjects. Similar to KCNQ1 S140G, the mutation had a gain-of-function effect on the KCNQ1-KCNE2 channel; unlike long QT syndrome-associated KCNE2 mutations, it did not alter HERG-KCNE2 current. The mutation did not alter the functions of the HCN channel family either. Thus, KCNE2 R27C is a gain-of-function mutation associated with the initiation and/or maintenance of AF.
  The American Journal of Human Genetics 12/2004; 75(5):899-905. · 10.60 Impact Factor
• Article: Higher-Derivative Gravitational Coupling Between Laser Beams

  Yihan Chen, Changgui Shao, Jiali Yan
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  ABSTRACT: The gravitational field due to laser pulse traveling along a straight waveguide with a velocity v c is considered in the framework of higher-derivative theory of gravitation. The deflection of a probe laser pulse propagating in the vicinity of a high-power laser pulse is discussed. It is shown from a numerical comparison that the deflection of the probe laser pulse predicted by higher-derivative theory of gravitation is much less than the prediction of general relativity if the wavelength of the laser pulse is smaller than the range of the additional force.
  General Relativity and Gravitation 03/2003; 35(4):567-578. · 2.07 Impact Factor