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Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease.
Medicine (Baltimore). 2016 Dec; 95(52):e5669.M

Abstract

As environmental risk factors (ERFs) play an important role in the pathogenesis of Kashin-Beck disease (KBD), it is important to identify the interaction between ERFs and differentially expression genes (DEGs) in KBD. The environmental response genes (ERGs) were analyzed in cartilage of KBD in comparison to normal controls.We searched 5 English and 3 Chinese databases from inception to September 2015, to identify case-control studies that examined ERFs for KBD using integrative meta-analysis and systematic review. Total RNA was isolated from articular cartilage of KBD patients and healthy controls. Human whole genome microarray chip (Agilent) was used to analyze the amplified, labeled, and hybridized total RNA, and the validated microarray data were partially verified using real-time quantitative polymerase chain reaction (qRT-PCR). The ERGs were derived from the Comparative Toxicogenomics Database. The identified ERGs were subjected to KEGG pathway enrichment, biological process (BP), and interaction network analyses using the Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.7, and STRING.The trace elements (selenium and iodine), vitamin E, and polluted grains (T-2 toxin/HT-2 toxin, deoxynivalenol, and nivalenol) were identified as the ERFs for KBD using meta-analysis and review. We identified 21 upregulated ERGs and 7 downregulated ERGs in cartilage with KBD compared with healthy controls, which involved in apoptosis, metabolism, and growth and development. KEGG pathway enrichment analysis found that 2 significant pathways were involved with PI3K-Akt signaling pathway and P53 signaling pathway, and gene ontology function analysis found 3 BPs involved with apoptosis, death, and cell death in KBD cartilage.According to previous results and our own research, we suggest that the trace element selenium and vitamin E induce PI3K-Akt signaling pathway and the mycotoxins (T-2 toxin/HT-2 toxin and DON) induce P53 signaling pathway, contributing to the development of KBD, and chondrocyte apoptosis and cell death.

Authors+Show Affiliations

aInstitute of Endemic Diseases, School of Public Health of Health Science Center, Xi'an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an bDepartment of Orthopedics, Baoji People's Hospital, Baoji, China cDepartment of Integrative Medical Biology, University of Umeå, Umeå, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Meta-Analysis
Review
Systematic Review

Language

eng

PubMed ID

28033256

Citation

Yu, Fang-Fang, et al. "Identified Molecular Mechanism of Interaction Between Environmental Risk Factors and Differential Expression Genes in Cartilage of Kashin-Beck Disease." Medicine, vol. 95, no. 52, 2016, pp. e5669.
Yu FF, Zhang YX, Zhang LH, et al. Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease. Medicine (Baltimore). 2016;95(52):e5669.
Yu, F. F., Zhang, Y. X., Zhang, L. H., Li, W. R., Guo, X., & Lammi, M. J. (2016). Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease. Medicine, 95(52), e5669. https://doi.org/10.1097/MD.0000000000005669
Yu FF, et al. Identified Molecular Mechanism of Interaction Between Environmental Risk Factors and Differential Expression Genes in Cartilage of Kashin-Beck Disease. Medicine (Baltimore). 2016;95(52):e5669. PubMed PMID: 28033256.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Identified molecular mechanism of interaction between environmental risk factors and differential expression genes in cartilage of Kashin-Beck disease. AU - Yu,Fang-Fang, AU - Zhang,Yan-Xiang, AU - Zhang,Lian-He, AU - Li,Wen-Rong, AU - Guo,Xiong, AU - Lammi,Mikko J, PY - 2016/12/30/entrez PY - 2016/12/30/pubmed PY - 2017/2/16/medline SP - e5669 EP - e5669 JF - Medicine JO - Medicine (Baltimore) VL - 95 IS - 52 N2 - As environmental risk factors (ERFs) play an important role in the pathogenesis of Kashin-Beck disease (KBD), it is important to identify the interaction between ERFs and differentially expression genes (DEGs) in KBD. The environmental response genes (ERGs) were analyzed in cartilage of KBD in comparison to normal controls.We searched 5 English and 3 Chinese databases from inception to September 2015, to identify case-control studies that examined ERFs for KBD using integrative meta-analysis and systematic review. Total RNA was isolated from articular cartilage of KBD patients and healthy controls. Human whole genome microarray chip (Agilent) was used to analyze the amplified, labeled, and hybridized total RNA, and the validated microarray data were partially verified using real-time quantitative polymerase chain reaction (qRT-PCR). The ERGs were derived from the Comparative Toxicogenomics Database. The identified ERGs were subjected to KEGG pathway enrichment, biological process (BP), and interaction network analyses using the Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.7, and STRING.The trace elements (selenium and iodine), vitamin E, and polluted grains (T-2 toxin/HT-2 toxin, deoxynivalenol, and nivalenol) were identified as the ERFs for KBD using meta-analysis and review. We identified 21 upregulated ERGs and 7 downregulated ERGs in cartilage with KBD compared with healthy controls, which involved in apoptosis, metabolism, and growth and development. KEGG pathway enrichment analysis found that 2 significant pathways were involved with PI3K-Akt signaling pathway and P53 signaling pathway, and gene ontology function analysis found 3 BPs involved with apoptosis, death, and cell death in KBD cartilage.According to previous results and our own research, we suggest that the trace element selenium and vitamin E induce PI3K-Akt signaling pathway and the mycotoxins (T-2 toxin/HT-2 toxin and DON) induce P53 signaling pathway, contributing to the development of KBD, and chondrocyte apoptosis and cell death. SN - 1536-5964 UR - https://www.unboundmedicine.com/medline/citation/28033256/Identified_molecular_mechanism_of_interaction_between_environmental_risk_factors_and_differential_expression_genes_in_cartilage_of_Kashin_Beck_disease_ L2 - http://dx.doi.org/10.1097/MD.0000000000005669 DB - PRIME DP - Unbound Medicine ER -