Arman Zhao

Publications (2)5.96 Total impact

• Article: Lack of support for association between the copy number variants in the FCGR locus and schizophrenia: a case control study.

  Arman Zhao, Yuqian Xiang, Jiawei Xu, Qiaoli Li, Lei Wang, Qinghe Xing, Zhou Zhang, Yun Liu, Guoyin Feng, Lin He, Xinzhi Zhao
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  ABSTRACT: The missing heritability of polygenic schizophrenia after genome-wide association studies (GWAS) can be potentially accounted for by the fact that most dynamic multiallelic copy number variants (CNVs) overlap segmental duplications (SDs). The FCGR locus covers this category of complex CNVs and it has long been postulated to harbor variants conferring the risk of schizophrenia. However, such association remains unproven. We used a case-control design to investigate CNV-based association with the disease. Data were obtained from 598 unrelated schizophrenia patients and 959 normal controls of Han ancestry from Shanghai. A total of four copy number (CN) probes in the FCGR locus were detected using TaqMan(®) Copy Number Assay. SPSS version 16.0 was used for the statistical analyses. And the frequency distributions of target CN in FCGR locus were very similar between controls and cases, whereas the CNV frequency differed markedly among different target CN analyzed in the two cohorts. When compared with the predominant two copies per diploid genome, a distinct non-protein-coding CN deletion region containing regulatory sequences was detected by probe Hs04194069_cn. Taken together, we found no evidence of association of target CNVs in the FCGR locus with schizophrenia. However, our negative findings suggest that more detailed next generation sequencing-based association studies are needed to fully evaluate the contribution of this category of complex CNVs to the disease.
  Neuroscience Letters 05/2012; 522(2):85-91. · 2.11 Impact Factor
• Article: Promoter hypomethylation of COMT in human placenta is not associated with the development of pre-eclampsia.

  Arman Zhao, Yan Cheng, Xiaotian Li, Qiaoli Li, Lei Wang, Jiawei Xu, Yuqian Xiang, Qinghe Xing, Lin He, Xinzhi Zhao
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  ABSTRACT: Disruption of the Catechol-O-methyltransferase (COMT) gene has been shown to be involved in pre-eclampsia (PE). To investigate whether two promoters of the COMT gene are differentially regulated by methylation in PE patients, we have analyzed the genomic DNA extracted from placenta (cases n = 16; controls n = 21), maternal peripheral blood (cases n = 4; controls n = 6) and umbilical cord blood (cases n = 8; controls n = 8) of women with PE and women with normal pregnancy. Bisulfite sequencing identified the predominantly unmethylated MB-COMT promoter in placenta, maternal peripheral blood and umbilical cord blood samples (PE and control). Subsequent quantitative MassArray data confirmed a significant tissue-specific hypomethylation of the S-COMT promoter in placenta (mean = 28.6%) when compared with its densely methylated patterns in blood samples (mean = 74.5%, P < 0.001), consistent with the sequencing data. However, no PE-specific methylation difference was found between cases and controls either in placenta or in blood samples. Moreover, none of the clinical characteristics had an effect on the methylation status of the S-COMT promoter. This study does not support a causal link between methylation regulation of COMT promoters and PE. However, the observed placenta-specific S-COMT promoter may be a potential marker for early prediction of PE in maternal plasma, although this remains to be further evaluated.
  Molecular Human Reproduction 11/2010; 17(3):199-206. · 3.85 Impact Factor