Guo-Ying Huang

Fudan University, Shanghai, Shanghai Shi, China

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Publications (58)154.25 Total impact

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    ABSTRACT: We aimed to compare the diagnostic value of indexed right ventricular end-diastolic volume (RVEDVi) and the ratio of right ventricle volume to left ventricle volume (RV/LV ratio) in prediction of the severity of pulmonary regurgitation (PR) expressed as the PR fraction (PRF) after surgery of tetralogy of Fallot (TOF). Forty-one patients with repaired TOF were included in the study. RVEDVi, LVEDVi, RV/LV ratio, PRF and ejection fraction were measured with magnetic resonance imaging. A PRF of more than 20% was considered significant. The predictive capability of two markers (RVEDVi and RV/LV ratio) for significant PR was compared using multivariate linear regression analysis and receiver operating characteristic (ROC) analysis. Both the RV/LV ratio and RVEDVi showed a correlation with PRF (r = 0.526/0.321, p = 0.001/0.041) in the correlation analysis, but in multivariate regression analysis the only independent predictor of PRF was the RV/LV ratio (F = 14.890, p = 0.001). ROC analysis revealed that a better discrimination of significant PR (>20%) from slight types (=20%) PR can be reached with the RV/LV ratio than RVEDVi (AUC = 0.805/0.709, p = 0.01). The RV/LV ratio was better than RVEDVi at differentiating mild from moderate PR (p = 0.006 vs. p = 0.153), and proved superior over RVEDVi in predicting PR based on the PRF criterion.
    Cardiology 11/2015; 133(3):135-140. DOI:10.1159/000441291 · 2.18 Impact Factor
  • Fei Liang · Lei Diao · Nan Jiang · Jin Zhang · Hui-Jun Wang · Wen-Hao Zhou · Guo-Ying Huang · Duan Ma ·
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    ABSTRACT: Although paternal ethanol (EtOH) abuse has been shown to affect the growth and behavior of offspring, the exact molecular and mechanistic basis remains largely unclear. Methylation alterations in imprinted genes may be related to well-documented teratogenic effects of ethanol. Here we show that chronic paternal ethanol exposure increases the susceptibility to abnormal behavior in offspring through male game epigenetic alteration. In our study, different doses of ethanol (0, 1.1, 3.3 g kg-1 ) were administered intra-gastrically to male mice and decreased sperm motility was found in the highest ethanol-exposed group compared with the controls. Data also showed a dose-dependent increase in deaf mice of the paternally ethanol-exposed groups. The methylation of H19, Peg3, Ndn and Snrpn was assessed in paternal spermatozoa and in the cerebral cortices of deaf mice. EtOH affected methylation of Peg3 (CpG 3, 7 and 9) in paternal spermatozoa and in the cerebral cortices of deaf mice, but the level of mRNA expression did not change, suggesting that other gene regulation may be involved in these processes. Overall, chronic paternal ethanol exposure could alter the methylation of imprinted genes in sire spermatozoa that could also be passed on to offspring, giving rise to developmental disorders. Our results provide possible epigenetic evidence for a paternal ethanol exposure contribution to Fetal Alcohol Syndrome (FAS).
    Asian Journal of Andrology 08/2015; 17(6). DOI:10.4103/1008-682X.160267 · 2.60 Impact Factor
  • Guo-Ying Huang · Xiao-Jing Ma · Jing Zhang ·

    Chinese medical journal 05/2015; 128(9):1277. DOI:10.4103/0366-6999.156156 · 1.05 Impact Factor
  • Fang Liu · Chun-Hua Qi · Lin Wu · Li-Feng Zhang · Lan He · Guo-Ying Huang ·
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    ABSTRACT: Background: Although balloon angioplasty (BA) has been performed for more than 20 years, its use as a treatment for native coarctation of the aorta (CoA) during childhood, especially in young infants, remains controversial. This study aimed to assess the effects and potential role of percutaneous transcatheter BA for native CoA as an alternative therapy to surgical repair in young infants. Methods: The 37 patients aged from 6 days to 6 months with severe CoA in congestive heart failure or circulatory shock were admitted for BA. Patient's weight ranged from 2.4 to 6.1 kg. All 37 patients were experiencing cardiac dysfunction, and eight patients were in cardiac shock with severe metabolic acidosis. Eleven patients had an isolated CoA, whereas the others had a CoA associated with other cardiac malformations. Cardiac catheterization and aortic angiography were performed under general anesthesia with intubation. Transfemoral arterial approaches were used for the BA. The size of the balloon ranged from 3 mm × 20 mm to 8 mm × 20 mm, and a coronary artery balloon catheter was preferred over a regular peripheral vascular balloon catheter. Results: The femoral artery was successfully punctured in all but one patient, with that patient undergoing a carotid artery puncture . The systolic peak pressure gradient (PG) across the coarctation was 41.0 ± 16.0 mmHg (range 13-76 mmHg). The mean diameter of the narrowest coarctation site was 1.7 ± 0.6 mm (range 0.5-2.8 mm). All patients had successful dilation; the PG significantly decreased to 13.0 ± 11.0 mmHg (range 0-40 mmHg), and the diameter of coarctation significantly improved to 3.8 ± 0.9 mm (range 2.5-5.3 mm). No intraoperative complications occurred for any patients. However, in one case that underwent a carotid artery puncture, a giant aneurysm formed at the puncture site and required surgical repair. The following observations were made during the follow-up period from 6-month to 7-year: (1) The PG across the coarctation measured by echocardiography further decreased or remained stable in 31 cases. The remaining six patients, whose PGs gradually increased, required a second dilation. No patient required further surgery because of a CoA; (2) in two cases, an aortic aneurysm was found with an angiogram performed immediately postdilatation and disappeared at 18 and 12 months of age, respectively; (3) tricuspid regurgitation and pulmonary hypertension improved in all patients; (4) all patients were doing well and were asymptomatic. Conclusions: Percutaneous BA is a relatively safe and effective treatment for severe native CoA in young infants, and should be considered a valid alternative to surgery because of its good outcome and less trauma and fewer complications than surgery.
    Chinese medical journal 04/2015; 128(8):1021. DOI:10.4103/0366-6999.155069 · 1.05 Impact Factor
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    ABSTRACT: Several pioneering studies have provided evidence for the introduction of universal pulse oximetry screening for critical congenital heart disease. However, whether the benefits of screening reported in studies from high-income countries would translate with similar success to low-income countries is unknown. We assessed the feasibility and reliability of pulse oximetry plus clinical assessment for detection of major congenital heart disease, especially critical congenital heart disease, in China.
    The Lancet 04/2014; 384(9945). DOI:10.1016/S0140-6736(14)60198-7 · 45.22 Impact Factor
  • Lin Yang · Hui-Jun Wang · Guo-Ying Huang · Wen-Hao Zhou ·
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    ABSTRACT: Congenital malformation is one of the most frequent causes of infant death in western countries and major cities in China. Though genetic screening of newborns remains a hot issue and concern, the mortality rate associated with birth defects has not been significantly reduced over the past 20 years. Many genetic diseases manifest symptoms during the first 28 days of life, but full clinical symptoms might not be evident in newborns. Moreover, genetic aberrations is highly heterogeneous. These complicated factors lead to the establishment of diagnosis based on nonspecific or obscure symptoms. Recently developed array comparative genomic hybridization (CGH) and next generation sequencing (NGS) techniques with efficient high-resolution allow to screening of the entire genome for DNA copy number variants and sequencing respectively. These new and powerful tools can shorten the differential diagnosis process and quicken to movement towards targeted treatment and genetic and prognostic counseling.
    Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 11/2013; 15(11):960-964. DOI:10.7499/j.issn.1008-8830.2013.11.008
  • Yao Wu · Xiao-Jing Ma · Hui-Jun Wang · Wen-Can Li · Long Chen · Duan Ma · Guo-Ying Huang ·
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    ABSTRACT: Abnormal expression of connexin 43 (Cx43) has been reported to play an important role in the development of conotrunccal anomalies. However, less is known about the underlying reason for its abnormal expression. MicroRNAs (miRNAs), as an important part of gene expression regulation, have been implicated in some cardiac diseases. This study aimed to investigate the expression of Cx43 and its related miRNAs in patients with tetralogy of Fallot (TOF), and illustrate the potential role of abnormal miRNAs regulation to Cx43 expression in the pathology of TOF. Real-time polymerase chain reaction (PCR) was used to detect the expression of Cx43 and 10 Cx43-related miRNAs in the myocardium from 30 TOF patients and 10 normal controls. Immunohistochemistry was used to detect Cx43 protein expression. Putative miRNA binding sites in the 3'UTR of Cx43 were examined in 200 TOF patients and 200 healthy individuals, using Sanger sequencing, to exclude sequence variations resulting in binding difficulties of miRNAs. Cx43 mRNA and protein expression in the myocardium tissue was significantly increased in TOF patients. The expression of MiR-1 and 206 was significantly decreased in the TOF patients as compared with the controls (P<0.05). No obvious difference was observed in the expression of the other 7 miRNAs between the TOF patients and controls (P>0.05). No meaningful sequence variation was detected in the putative miR1/206 binding sites in the 3'UTR of Cx43. This study indicated that miR-1 and 206 is down-regulated in TOF patients, which may cause an up-regulation of Cx43 protein's synthesis. It provided a clue that miR-1 and 206 might be involved in the pathogenesis of TOF, additional experiments are needed to determine if in fact, miR-1 and 206 contribute substantially to TOF.
    World Journal of Pediatrics 10/2013; 10(2). DOI:10.1007/s12519-013-0434-0 · 1.05 Impact Factor
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    ABSTRACT: Tetralogy of Fallot (TOF) is 1 of the most common heart defects in children, and the underlying mechanisms remain largely elusive. MicroRNAs (miRNAs) are a class of regulators of gene expression and are increasingly recognized for their roles in heart development. To identify miRNAs abnormally expressed in TOF, microarrays were used to analyze the miRNA expression profiles of 5 samples of myectomy tissues from right ventricular outflow tract (RVOT) obstruction of infants with nonsyndromic TOF and 3 age-matched normal RVOT tissues. In total, 41 candidate miRNAs were identified. To further validate the microarray results, the 41 miRNAs were detected using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in a larger independent population of tissue samples, including 21 from patients with TOF and 6 from normal controls; it was found that 18 miRNAs were expressed at significantly different levels. Bioinformatic analysis revealed that these miRNAs targeted a network of genes involved in heart development and human congenital heart diseases. Further in vitro studies indicated that upregulation of miR-424/424* promoted proliferation and inhibited migration of primary embryonic mouse cardiomyocytes, whereas miR-222 promoted cardiomyocyte proliferation and reduced the cardiomyogenic differentiation of P19 cells. The 3'UTR (3' untranslated region) luciferase assay revealed that miR-424/424* suppressed the expression of HAS2 and NF1, and their mRNAs were underexpressed in the RVOT myocardial tissues of TOF. Eighteen miRNAs were identified as being deregulated in RVOT myocardial tissues from infants with nonsyndromic TOF, and in vitro experiments indicated that miR-424/424* and miR-222 are involved in cardiomyocyte proliferation and migration and the cardiomyogenic differentiation of P19 cells.
    The Canadian journal of cardiology 10/2013; 29(12). DOI:10.1016/j.cjca.2013.07.002 · 3.94 Impact Factor
  • Jun Xu · Yi-Xiang Lin · Ruo-Yi Gu · Hui-Jun Wang · Xiao-Jing Ma · Duan Ma · Guo-Ying Huang ·
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    ABSTRACT: To study the expression of histone acetyltransferases (HATs) and histone deacetylases (HDACs) in children with tetralogy of Fallot (TOF), and to investigate the role of histone acetylation and acetylation-related enzymes in the pathogenesis of TOF. Myocardial tissue samples in the TOF group were obtained from 46 children with TOF who underwent radical operation, and myocardial tissue samples in the control group were obtained from 16 children who suffered accidental deaths and had no cardiac anomalies as shown by autopsy. The acetylation of H3K9, H3K18 and H3K27 was evaluated by immunohistochemistry. The mRNA expression of HATs and HDACs in the myocardium was measured by real-time PCR. The correlation between mRNA expression of HATs and HDACs and histone acetylation was analyzed. Compared with the control group, the TOF group showed significantly increased acetylation of H3K9 (P=0.0165) and significantly decreased acetylation of H3K18 (P=0.0048) and H3K27 (P=0.0084). As to 4 HATs and 6 HDACs, the mRNA expression of EP300 and CBP was significantly higher in the TOF group than in the control group (P=0.025; P=0.017), and there was no significant difference in the mRNA expression of other HATs and HDACs between the two groups. The correlation analysis revealed a positive correlation between H3K9 acetylation and mRNA expression of EP300 (r=0.71, P<0.01) and CBP (r=0.72, P<0.01). Upregulated mRNA expression of EP300 and CBP may be associated with increased H3K9 acetylation, suggesting that EP300 and CBP might affect cardiac development by regulating H3K9 acetylation.
    Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 10/2013; 15(10):817-821. DOI:10.7499/j.issn.1008-8830.2013.10.003
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    Lin Yang · Guo-Dong Zhan · Jun-Jie Ding · Hui-Jun Wang · Duan Ma · Guo-Ying Huang · Wen-Hao Zhou ·
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    ABSTRACT: Several studies have suggested a difference in clinical features of intellectual ability and psychiatric illness in the Prader-Willi syndrome (PWS) with the 15q11-q13 paternal deletion and maternal uniparental disomy (mUPD). Our objective was to appraise evidence on this association through a meta-analysis. The electronic records PubMed and EMBASE from 1956 to 2012 were extracted for meta-analysis. Meta-analyses were performed by using fixed effect model. Mean difference, odds ratio, and 95% confidence interval were calculated. We retrieved a total of 744 PWS cases from 13 studies. These include 423 cases with paternal 15q11-q13 deletions and 318 cases of mUPD. Compare to the PWS cases with mUPD, PWS patients with the paternal 15q11-q13 deletion associated with significantly lower full scale IQ (FSIQ) [mean difference (MD), -2.69; 95%CI, -4.86 to -0.52; p=0.02] and verbal IQ (VIQ) (MD, -7.5; 95%CI, -9.75 to -5.26; p<0.00001) but higher performance IQ (PIQ) (MD, 4.02; 95%CI, 1.13 to 6.91; p=0.006). In contrast, PWS patients with mUPD are associated with significantly higher risk of psychiatric illness [odds rate (OR), 0.14; 95%CI, 0.08 to 0.23; p<0.00001] and higher risk of bipolar disorder (OR, 0.04; 95%CI, 0.01 to 0.23; p=0.0002). Significant different clinical features of cognitive development and psychiatric illness are associated with PWS with different molecular defects. These findings provide support for evidence based practice to evaluate and manage the PWS syndrome with different molecular defects.
    PLoS ONE 08/2013; 8(8):e72640. DOI:10.1371/journal.pone.0072640 · 3.23 Impact Factor
  • Lan He · Fang Liu · Guo-Ying Huang ·

    Chinese medical journal 08/2013; 126(16):3192. DOI:10.3760/cma.j.issn.0366-6999.20123070 · 1.05 Impact Factor
  • Ying Lu · Lin Wu · Fang Liu · Xi-Hong Hu · Chun-Hua Qi · Lan He · Guo-Ying Huang ·
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    ABSTRACT: To characterize the clinical and angiographic features in children with renovascular hypertension. Clinical data of 14 children (7 male, 7 female; age 0.8-14 years, mean 8.7 years), who were diagnosed with renovascular hypertension by renal angiography in our institute from January 2005 to December 2012 were collected and retrospectively analyzed. The mean blood pressure at the diagnosis was 187/127 mm Hg. Chief complaints of symptomatic patients were headache (29%, 4/14), hypertensive encephalopathy (36%, 5/14), signs of congestive heart failure (14%, 2/14) and hematemesis (7%, 1/14). Renovascular hypertension was found incidentally in 14% (2/14) of patients who were asymptomatic. Conventional renal angiography elucidated the anatomical distribution of lesions in the renal arterial system. It was found that 14% (2/14) of patients had bilateral disease, 50% (7/14) had single stenosis at main or accessory renal artery, while multiple stenoses was seen in 43% (6/14) of children, with involvement of segmental renal artery and small interlobar or arcuate vessels. Compared with catheter angiography, 50% (7/14) of patients with renovascular hypertension, especially intrarenal arterial disease, were missed on computed tomography angiography or magnetic resonance angiography. It is mandatory to emphasize blood pressure measurement in pediatric clinical practice for early recognition of renovascular hypertension. As children with renovascular hypertension display involvement of multiple arteries, including in smaller intrarenal arteries, digital subtraction angiography is the only method that can reliably diagnose pediatric renovascular hypertension.
    Zhonghua er ke za zhi. Chinese journal of pediatrics 08/2013; 51(8):621-4.
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    ABSTRACT: Myocardial fibrosis plays a pivotal role in the development of heart failure. Hydrogen sulfide (H2S) is an endogenous gasotransmitter with potent cardioprotective properties; however, whether H2S is involved in fibrotic process remains unknown. This study aimed to explore the role of H2S in the process of cardiac fibrosis and the underlying mechanisms. Myocardial infarction (MI) was established in rats by ligation of coronary artery. Activation of rat neonatal cardiac fibroblasts was induced by angiotensin II (Ang II). Fibrotic responses in ischemic myocardium and in Ang II-stimulated cardiac fibroblasts were examined. The effects of sodium hydrosulfide (NaHS, an exogenous H2S donor) on NADPH oxidase 4 (Nox4), reactive oxygen species (ROS) production, extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation, heme oxygenase-1 (HO-1), and cystathionine γ-lyase (CSE) were tested to elucidate the protective mechanisms of H2S on fibrotic response. NaHS treatment inhibited Ang II-induced expression of α-smooth muscle actin, connective tissue growth factor (CTGF), and type I collagen and upregulated expression of HO-1 in cardiac fibroblasts. Ang II-induced Nox4 expression in cardiac fibroblasts was quenched by NaHS and this was associated with a decreased ROS production and reduced ERK1/2 phosphorylation and CTGF expression. In vivo studies using MI model indicated that NaHS administration attenuated Nox4 expression and fibrotic response. Moreover, NaHS therapy also prevented cardiac inflammatory response accompanied by increases in HO-1 and CSE expression. The beneficial effect of H2S, at least in part, was associated with a decrease of Nox4-ROS-ERK1/2 signaling axis and an increase in HO-1 expression.
    International journal of cardiology 07/2013; 168(4). DOI:10.1016/j.ijcard.2013.06.007 · 4.04 Impact Factor
  • Xiao-Jing Ma · Guo-Ying Huang ·
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    ABSTRACT: Life-threatening critical congenital heart disease (cCHD) is often not detected in the neonatal period. Unrecognized cCHD results in high morbidity and mortality rates. As a non-invasive, convenient, quick and accurate measuring method, pulse oximetry is considered to be a promising strategy to screen for cCHD in neonates. This article is a review on the neonatal pulse oximetry screening for cCHD. Articles on neonatal pulse oximetry screening for cCHD were accessed from PubMed, using keywords including congenital heart defects, neonatal screening and oximetry. Original articles and critical reviews selected were relevant to the review's theme. The factors in the course of implementation, including threshold for positive pulse-oximetry screening results, the pulse oximeters used, timing of the screening, and the measuring position, influence the accuracy of the screening. It is recommended that the screening is completed on the second day of life, before hospital discharge. Motion-tolerant pulse oximeters, which can also be applied to measure the saturation in low-perfusion conditions, should be used. The probe should be put on both the right hand and on one foot. Thresholds of < 95% in either limb or a difference of > 3% between the limbs as a positive result may be appropriate. It should be emphasized that pulse-oximetry screening cannot be used as the only way to detect cCHD, clinical examination is also important in this situation. Cost-benefit analysis in the United Kingdom revealed it was plausible to use pulse oximetry as an adjunct to clinical examination. However, it is still controversial as to whether pulse oximetry can be used as a routine screening method for cCHD in neonates. Neonatal pulse oximetry screening improves detection of cCHD. Further studies should be carried out before it becomes one of the routine newborn screening programs.
    Chinese medical journal 07/2013; 126(14):2736-40. DOI:10.3760/cma.j.issn.0366-6999.20122371 · 1.05 Impact Factor
  • Xi-Hong Hu · Mi-Er Pa · Quan-Li Shen · Guo-Ying Huang ·

    Chinese medical journal 07/2013; 126(14):2790-2. · 1.05 Impact Factor
  • Jun Xu · Hui-Jun Wang · Guo-Ying Huang ·

    Zhonghua er ke za zhi. Chinese journal of pediatrics 07/2013; 51(7):552-554.
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    ABSTRACT: Elevated homocysteine levels are known to be a risk factor for congenital heart disease (CHD), but the mechanism underlying this effect is unknown. During early embryonic development, homocysteine removal is dictated exclusively by the MTR activity. To examine the role of MTR in CHD risk, we identified genetic variants in MTR and investigated the mechanisms that affect its expression levels and that increase the risk of CHD in Chinese populations. The association between regulatory variants of the MTR gene and CHD was examined in three independent case-control studies in a total of 2340 patients with CHD and 2270 controls. The functional consequences of these variants were demonstrated using dual-luciferase assays, real-time polymerase chain reaction (PCR), electrophoretic mobility shift assays, surface plasma resonance, chromatin immunoprecipitation, and bisulfite sequencing, as well as by a group of predicted microRNAs using a gene reporter system. Two regulatory variants of MTR, -186T>G and +905G>A, were associated with an increased risk of CHD in both the separate and combined case-control studies (-186GG P = 1.32 × 10(-9); +905AA P = 6.35 × 10(-14)). Compared with the major allele, the -186G allele exhibited significantly lower promoter activity, decreased hnRNA and mRNA levels, reduced transcription factor binding affinity, and a more highly methylated promoter. The +905A allele exhibited a statistically stronger binding affinity to functional microRNAs that down regulate MTR expression at the translational level. Both of the minor alleles were correlated with elevated plasma homocysteine concentrations, indicating a genetic component for hyperhomocysteinaemia. Regulatory variants of the MTR gene increase CHD risk by reducing MTR expression and inducing the homocysteine accumulation and elevation.
    European Heart Journal 06/2013; 35(11). DOI:10.1093/eurheartj/eht221 · 15.20 Impact Factor
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    ABSTRACT: Background: MicroRNAs (miRNAs) are endogenous noncoding RNAs of approximately 22 nucleotides in length that mediate post-transcriptional gene silencing by annealing to sequences in the 3'-untranslated region of target mRNAs. Methods: In this study, we analyzed 25 candidate miRNAs selected based on microarray data for cardiac tissue from individuals with congenital heart defects (CHDs) and from healthy control tissue. Results: This study identified specific changes in the miR-1-1 and miR-181c levels in human cardiac samples from individuals with ventricular septal defects (VSDs) relative to the levels in healthy control tissue. Increased levels of GJA1 and SOX9 were associated with the decreased expression of miR-1-1 in VSD patients, and increased miR-181c expression was correlated with downregulated BMPR2 levels. In addition, the results revealed that miR-1-1 and miR-181c directly regulate the expression of these predicted targets. Conclusions: miR-1-1 and miR-181c are associated with the pathogenesis of VSDs.
    International journal of cardiology 01/2013; 168(2). DOI:10.1016/j.ijcard.2012.12.048 · 4.04 Impact Factor
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    ABSTRACT: Homocysteine is an independent risk factor for various cardiovascular diseases. There are two ways to remove homocysteine from embryonic cardiac cells: remethylation to form methionine or transsulfuration to form cysteine. Cystathionine β-synthase (CBS) catalyzes the first step of homocysteine transsulfuration as a rate-limiting enzyme. In this study, we identified a functional variant -4673C>G (rs2850144) in the CBS gene promoter region that significantly reduces the susceptibility to congenital heart disease (CHD) in a Han Chinese population consisting of 2 340 CHD patients and 2 270 controls. Individuals carrying the heterozygous CG and homozygous GG genotypes had a 15% (odds ratio (OR) = 0.85, 95% confidence interval (CI) = 0.75-0.96, P = 0.011) and 40% (OR = 0.60, 95% CI = 0.49-0.73, P = 1.78 × 10(-7)) reduced risk to develop CHD than the wild-type CC genotype carriers in the combined samples, respectively. Additional stratified analyses demonstrated that CBS -4673C>G is significantly related to septation defects and conotruncal defects. In vivo detection of CBS mRNA levels in human cardiac tissues and in vitro luciferase assays consistently showed that the minor G allele significantly increased CBS transcription. A functional analysis revealed that both the attenuated transcription suppressor SP1 binding affinity and the CBS promoter hypomethylation specifically linked with the minor G allele contributed to the remarkably upregulated CBS expression. Consequently, the carriers with genetically increased CBS expression would benefit from the protection due to the low homocysteine levels maintained by CBS in certain cells during the critical heart development stages. These results shed light on unexpected role of CBS and highlight the importance of homocysteine removal in cardiac development.Cell Research advance online publication 18 September 2012; doi:10.1038/cr.2012.135.
    Cell Research 09/2012; 23(2). DOI:10.1038/cr.2012.135 · 12.41 Impact Factor
  • Wei-Cheng Chen · Ying Zhang · Duan Ma · Xiao-Jing Ma · Wei-Nian Shou · Guo-Ying Huang ·
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    ABSTRACT: Epicardium-derived cells (EPDCs) can migrate into the myocardium, giving rise to several types of cell which are indispensable to compact myocardium and inducing normal myocardial development. Subepicardium accumulates bone morphogenetic proteins (Bmps), which can release into myocardium further. It has been shown that reduced Bmp-mediated signaling in a novel neural crest derivative in the epicardium reduced the cardiomyocyte proliferative activity in the developing myocardium. Furthermore, studies have demonstrated that cardiomyocytes can develop in proepicardial organ (PEO) explant cultures after stimulation with bone morphogenetic protein (Bmp2). We present a hypothesis that Bmp2 regulates the interaction between EPDCs and cardiomyocyte in the developing outflow tract (OFT). Our previous empirical data also shows that Bmp2 is expressed in the myocardial cell in the OFT at embryonic day (E) 14.5 in wild-type mice, and expression of Bmp2 in Cx43α1 knockout (KO) OFT was delayed for 1day. Further validation of this hypothesis will provide additional insight of the molecular mechanism of myocardium maturation.
    Medical Hypotheses 05/2012; 79(2):174-7. DOI:10.1016/j.mehy.2012.04.027 · 1.07 Impact Factor

Publication Stats

370 Citations
154.25 Total Impact Points


  • 2003-2014
    • Fudan University
      • • Institutes of Biomedical Sciences
      • • School of Life Sciences
      • • Department of Pediatrics
      Shanghai, Shanghai Shi, China
  • 2007
    • Shanghai's Children's Medical Center
      Shanghai, Shanghai Shi, China