Publications by authors named "Yingchao Zhou"

6 Publications

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Genetic association analysis between IL9 and coronary artery disease in a Chinese Han population.

Cytokine 2021 Nov 20;150:155761. Epub 2021 Nov 20.

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

Interleukin-9 (IL-9) plays important role in coronary artery disease (CAD). However, the exact relationship between them is not explored yet. Here, four tag SNPs covering IL9 (rs31563, rs2069868, rs2069870 and rs31564) were selected to conduct case-control association analyses in a total of 3704 individuals from Chinese Han population (1863 CAD vs 1841 control). Results showed that: first, rs2069868 was associated with CAD combined with hypertension (P = 0.027); second, IL9 haplotype (CGAT) was associated with CAD (P = 0.035), and the combination genotype of "rs31563_CC/rs31564_TT" would remarkably decrease the risk of CAD (P = 0.001); third, significant associations were found between rs2069870 and decreased LDL-c levels and decreased total cholesterol levels, and between rs31563 and increased HDL-c levels (P < 0.05). Therefore, we conclude that IL9 might play a causal role in CAD by interacted with CAD traditional risk factors, which might confer a new way to improve the prevention and treatment of CAD.
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http://dx.doi.org/10.1016/j.cyto.2021.155761DOI Listing
November 2021

Inhibition of miR-21 alleviated cardiac perivascular fibrosis via repressing EndMT in T1DM.

J Cell Mol Med 2020 01 3;24(1):910-920. Epub 2019 Nov 3.

Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, China.

In type 1 and type 2 diabetes mellitus, increased cardiac fibrosis, stiffness and associated diastolic dysfunction may be the earliest pathological phenomena in diabetic cardiomyopathy. Endothelial-mesenchymal transition (EndMT) in endothelia cells (ECs) is a critical cellular phenomenon that increases cardiac fibroblasts (CFs) and cardiac fibrosis in diabetic hearts. The purpose of this paper is to explore the molecular mechanism of miR-21 regulating EndMT and cardiac perivascular fibrosis in diabetic cardiomyopathy. In vivo, hyperglycaemia up-regulated the mRNA level of miR-21, aggravated cardiac dysfunction and collagen deposition. The condition was recovered by inhibition of miR-21 following with improving cardiac function and decreasing collagen deposition. miR-21 inhibition decreased cardiac perivascular fibrosis by suppressing EndMT and up-regulating SMAD7 whereas activating p-SMAD2 and p-SMAD3. In vitro, high glucose (HG) up-regulated miR-21 and induced EndMT in ECs, which was decreased by inhibition of miR-21. A highly conserved binding site of NF-κB located in miR-21 5'-UTR was identified. In ECs, SMAD7 is directly regulated by miR-21. In conclusion, the pathway of NF-κB/miR-21/SMAD7 regulated the process of EndMT in T1DM, in diabetic cardiomyopathy, which may be regarded as a potential clinical therapeutic target for cardiac perivascular fibrosis.
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http://dx.doi.org/10.1111/jcmm.14800DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6933373PMC
January 2020

Type I Diabetic Akita Mouse Model is Characterized by Abnormal Cardiac Deformation During Early Stages of Diabetic Cardiomyopathy with Speckle-Tracking Based Strain Imaging.

Cell Physiol Biochem 2018 21;45(4):1541-1550. Epub 2018 Feb 21.

Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, China.

Background/aims: Diabetes mellitus (DM) has been demonstrated to have a strong association with heart failure. Conventional echocardiographic analysis cannot sensitively monitor cardiac dysfunction in type I diabetic Akita hearts, but the phenotype of heart failure is observed in molecular levels during the early stages.

Methods: Male Akita (Ins2WT/C96Y) mice were monitored with echocardiographic imaging at various ages, and then with conventional echocardiographic analysis and speckle-tracking based strain analyses.

Results: With speckle-tracking based strain analyses, diabetic Akita mice showed changes in average global radial strain at the age of 12 weeks, as well as decreased longitudinal strain. These changes occurred in the early stage and remained throughout the progression of diabetic cardiomyopathy in Akita mice. Speckle-tracking showed that the detailed and precise changes of cardiac deformation in the progression of diabetic cardiomyopathy in the genetic type I diabetic Akita mice were uncoupled.

Conclusions: We monitored early-stage changes in the heart of diabetic Akita mice. We utilize this technique to elucidate the underlying mechanism for heart failure in Akita genetic type I diabetic mice. It will further advance the assessment of cardiac abnormalities, as well as the discovery of new drug treatments using Akita genetic type I diabetic mice.
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http://dx.doi.org/10.1159/000487690DOI Listing
May 2018

De Novo (Fibroblast Growth Factor 12) Functional Variation Is Potentially Associated With Idiopathic Ventricular Tachycardia.

J Am Heart Assoc 2017 Aug 3;6(8). Epub 2017 Aug 3.

Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, China

Background: Idiopathic ventricular tachycardia (VT) is a type of cardiac arrhythmia occurring in structurally normal hearts. The heritability of idiopathic VT remains to be clarified, and numerous genetic factors responsible for development of idiopathic VT are as yet unclear. Variations in (fibroblast growth factor 12), which is expressed in the human ventricle and modulates the cardiac Na channel Na1.5, may play an important role in the genetic pathogenesis of VT.

Methods And Results: We tested the hypothesis that genetic variations in are associated with VT in 2 independent Chinese cohorts and resequenced all the exons and exon-intron boundaries and the 5' and 3' untranslated regions of in 320 unrelated participants with idiopathic VT. For population-based case-control association studies, we chose 3 single-nucleotide polymorphisms-rs1460922, rs4687326, and rs2686464-which included all the exons of . The results showed that the single-nucleotide polymorphism rs1460922 in was significantly associated with VT after adjusting for covariates of sex and age in 2 independent Chinese populations: adjusted =0.015 (odds ratio: 1.54 [95% CI, 1.09-2.19]) in the discovery sample, adjusted =0.018 (odds ratio: 1.64 [95% CI, 1.09-2.48]) in the replication sample, and adjusted =2.52E-04 (odds ratio: 1.59 [95% CI, 1.24-2.03]) in the combined sample. After resequencing all amino acid coding regions and untranslated regions of , 5 rare variations were identified. The result of western blotting revealed that a de novo functional variation, p.P211Q (1.84% of 163 patients with right ventricular outflow tract VT), could downregulate expression significantly.

Conclusions: In this study, we observed that rs1460922 of was significantly associated with VT and identified that a de novo variation of may be an important genetic risk factor for the pathogenesis of VT.
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http://dx.doi.org/10.1161/JAHA.117.006130DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5586455PMC
August 2017

Genomic Variant in IL-37 Confers A Significant Risk of Coronary Artery Disease.

Sci Rep 2017 02 9;7:42175. Epub 2017 Feb 9.

Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Center for Human Genome Research, Cardio-X Institute, Huazhong University of Science and Technology, Wuhan, P. R. China.

The interleukin 1 family plays an important role in the immune and inflammatory responses. Coronary artery disease (CAD) is a chronic inflammatory disease. However, the genetic association between IL-37, the seventh member of the IL-1 family, and CAD is unknown. Here we show that a single nucleotide polymorphism in the IL-37 gene (rs3811047) confers a significant risk of CAD. We have performed an association analysis between rs3811047 and CAD in two independent populations with 2,501 patients and 3,116 controls from China. Quantitative RT-PCR analysis has been performed to determine if the IL-37 expression level is influenced by rs3811047. We show that the minor allele A of rs3811047 is significantly associated with CAD in two independent populations under a recessive model (P = 5.51 × 10/OR = 1.56 in the GeneID Northernern population and P = 1.23 × 10/OR = 1.45 in the GeneID Central population). The association became more significant in the combined population (P = 9.70 × 10/OR = 1.47). Moreover, the association remains significant in a CAD case control population matched for age and sex. Allele A of rs3811047 shows significant association with a decreased mRNA expression level of IL-37 (n = 168, P = 3.78 × 10). These data suggest that IL37 is a new susceptibility gene for CAD, which provides a potential target for the prevention and treatment of CAD.
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http://dx.doi.org/10.1038/srep42175DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5299598PMC
February 2017

Regulation of CARD8 expression by ANRIL and association of CARD8 single nucleotide polymorphism rs2043211 (p.C10X) with ischemic stroke.

Stroke 2014 Feb 2;45(2):383-8. Epub 2014 Jan 2.

From the Key Laboratory of Molecular Biophysics of the Ministry of Education, Cardio-X Institute (Y.B., G.J., Yingchao Zhou, M.Z., Yuanyuan Zhao, S.L., F.W., Q. Lu, Y.H., Q.Y., T.K., H.L., X.R., C.X., X.T., Q.K.W.), and College of Life Science and Technology and Center for Human Genome Research, Institute of Cardiology (S.N., X.C., Y. Liao), Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiology, Jining Medical College Affiliated Hospital, Jining, China (Q. Li); Department of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, China (Y. Li); Department of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, China (Y.X., Y. Liu, J.L., Y.Y.); Department of Cardiology, Suizhou Central Hospital, Suizhou, China (J.Q.); Department of Cardiology, Xiangyang Central Hospital, Xiangyang, China (B.L.); Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China (G.W.); Department of Cardiology, Wuhan No. 1 Hospital, Wuhan, China (Y.W.); Research Institute of the National Population and Family Planning Commission, Beijing, China (B.W., X.M.); and Department of Molecular Cardiology, Center for Cardiovascular Genetics, Lerner Research Institute, Cleveland Clinic, OH (Q.K.W.).

Background And Purpose: ANRIL has long been considered as the strongest candidate gene at the 9p21 locus, robustly associated with stroke and coronary artery disease. However, the underlying molecular mechanism remains unknown. The present study works to elucidate such a mechanism.

Methods: Using expression quantitative loci analysis, we identified potential genes whose expression may be influenced by genetic variation in ANRIL. To verify the identified gene(s), knockdown and overexpression of ANRIL were evaluated in human umbilical vein endothelial cells and HepG2 cells. Ischemic stroke and coronary artery disease risk were then evaluated in the gene(s) demonstrated to be mediated by ANRIL in 3 populations of Chinese Han ancestry: 2 ischemic stroke populations consisting of the Central China cohort (903 cases and 873 controls) and the Northern China cohort (816 cases and 879 controls) and 1 coronary artery disease cohort consisting of 772 patients and 873 controls.

Results: Expression quantitative loci analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and overexpression of ANRIL increasing CARD8 expression. The minor T allele of a previously identified CARD8 variant (rs2043211) was found to be significantly associated with a protective effect of ischemic stroke under the recessive model in 2 independent stroke cohorts. No significant association was found between rs2043211 and coronary artery disease.

Conclusions: CARD8 is a downstream target gene regulated by ANRIL. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.
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http://dx.doi.org/10.1161/STROKEAHA.113.003393DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962686PMC
February 2014
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