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Disease embryo development network reveals the relationship between disease genes and embryo development genes.

ABSTRACT: A basic problem for contemporary biology and medicine is exploring the correlation between human disease and underlying cellular mechanisms. For a long time, several efforts were made to reveal the similarity between embryo development and disease process, but few from the system level. In this article, we used the human protein-protein interactions (PPIs), disease genes with their classifications and embryo development genes and reconstructed a human disease-embryo development network to investigate the relationship between disease genes and embryo development genes. We found that disease genes and embryo development genes are prone to connect with each other. Furthermore, diseases can be categorized into three groups according to the closeness with embryo development in gene overlapping, interacting pattern in PPI network and co-regulated by microRNAs or transcription factors. Embryo development high-related disease genes show their closeness with embryo development at least in three biological levels. But it is not for embryo development medium-related disease genes and embryo development low-related disease genes. We also found that embryo development high-related disease genes are more central than other disease genes in the human PPI network. In addition, the results show that embryo development high-related disease genes tend to be essential genes compared with other diseases' genes. This network-based approach could provide evidence for the intricate correlation between disease process and embryo development, and help to uncover potential mechanisms of human complex diseases.

SUBMITTER: Gong B

PROVIDER: S-EPMC7094120 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature

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Disease embryo development network reveals the relationship between disease genes and embryo development genes.

Gong Binsheng B Liu Tao T Zhang Xiaoyu X Chen Xi X Li Jiang J Lv Hongchao H Zou Yi Y Li Xia X Rao Shaoqi S

Journal of theoretical biology 20110803

A basic problem for contemporary biology and medicine is exploring the correlation between human disease and underlying cellular mechanisms. For a long time, several efforts were made to reveal the similarity between embryo development and disease process, but few from the system level. In this article, we used the human protein-protein interactions (PPIs), disease genes with their classifications and embryo development genes and reconstructed a human disease-embryo development network to invest ...[more]

PMID: 21824480

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Project description:Coronary artery disease (CAD) is the principal cause of death in patients with nonalcoholic fatty liver disease (NAFLD). The aim of the present study was to investigate whether NAFLD is causally involved in the pathogenesis of CAD. For this, previously reported NAFLD susceptibility genes were clustered and tested for an association with CAD in the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis plus the Coronary Artery Disease Genetics (CARDIoGRAMplusC4D) Consortium data set. The role of plasma lipids as a potential mediator was explored by using data from the Global Lipids Genetics Consortium. Statistical analyses revealed that the combination of 12 NAFLD genes was not associated with CAD in 60,801 CAD cases and 123,504 controls (odds ratio [OR] per NAFLD risk allele, 1.0; 95% confidence interval [CI], 0.99-1.00). In a subsequent sensitivity analysis, a positive relationship was observed after exclusion of gene variants that are implicated in NAFLD through impaired very low-density lipoprotein secretion (i.e., microsomal triglyceride transfer protein [MTTP], patatin-like phospholipase domain containing 3 [PNPLA3], phosphatidylethanolamine N-methyltransferase [PEMT], and transmembrane 6 superfamily member 2 [TM6SF2]) (OR, 1.01; 95% CI, 1.00-1.02). Clustering of the excluded genes showed a significant negative relationship with CAD (OR, 0.97; 95% CI, 0.96-0.99). A substantial proportion of the observed heterogeneity between the individual NAFLD genes in relation to CAD could be explained by plasma lipids, as reflected by a strong relationship between plasma lipids and CAD risk conferred by the NAFLD susceptibility genes (r = 0.76; P = 0.004 for low-density lipoprotein cholesterol). Conclusion: NAFLD susceptibility genes do not cause CAD per se. The relationship between these genes and CAD appears to depend to a large extent on plasma lipids. These observations strongly suggest taking plasma lipids into account when designing a new drug to target NAFLD.

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Disease embryo development network reveals the relationship between disease genes and embryo development genes.

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Disease embryo development network reveals the relationship between disease genes and embryo development genes.

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