| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Huang, Y. Y. Chuang, S. Y. Wang, C. C. Lin, C. Yang, H. Y. Su, W. Chen, C. Y. Su, S. L. Fang, W. H. Chu, M. Y. Huang, G. S. Yang, Y. T. |
| Description |
Country affiliation: China Author Affiliation: Yang HY ( School of Public Health, National Defense Medical Center, Taipei, Taiwan, China.); Chuang SY ( Department of Orthopedics, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan, China.); Fang WH ( Department of Family and Community Medicine, Tri-Service General Hospital, Taipei, Taiwan, China.); Huang GS ( Department of Radiology, Tri-Service General Hospital, Taipei, Taiwan, China.); Wang CC ( Department of Orthopedics, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan, China.); Huang YY ( School of Public Health, National Defense Medical Center, Taipei, Taiwan, China.); Chu MY ( Department of Aviation Medicine and Physical Examination, National Defense Medical Center Tri-Service General Hospital Songshan Branch, Taipei, Taiwan, China.); Lin C ( Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, China.); Su W ( Department of Nursing, Chang Gung University of Science and Technology, Taoyuan, Taiwan, China.); Chen CY ( Division of Radiology, National Defense Medical Center Tri-Service General Hospital Songshan Branch, Taipei, Taiwan, China.); Yang YT ( School of Public Health, National Defense Medical Center, Taipei, Taiwan, China.); Su SL ( School of Public Health, National Defense Medical Center, Taipei, Taiwan, China.) |
| Abstract |
Recent studies have revealed that the inflammatory process plays a role in the pathogenesis of osteoarthritis (OA). The S100 family and receptor for advanced glycation end products (RAGE) participate in regulating inflammation, even in the production of matrix metalloproteinases (MMPs). MMP-1 degrades cartilage, which may result in OA development. Moreover, polymorphisms in RAGE, S100A8, and MMP-1 have a marked effect on ligand binding and transcription regulating. In this study, we investigated the potential genetic contribution of the RAGE, S100A8, and MMP-1 genes to OA. We performed a matched case-control association study and genotyped OA patients and healthy controls, who were analyzed by polymerase chain reaction-restriction fragment length polymorphism assays. A total of 207 patients were diagnosed with knee OA and underwent total knee replacement. The control group included 207 individuals who had standard X-rays of the knee joints to confirm K/L < 2 and were matched by age and gender. Single-nucleotide polymorphisms in RAGE (-429T/C, -374T/A, and 557G/A), S100A8 (rs3795391A/G), and MMP-1 (-1607 1G/2G, -755G/T, and -519A/G) were evaluated. RAGE -374T/A, S100A8 rs3795391A/G, MMP-1 -1607 1G/2G, -755G/T, and -519A/G showed no significant difference between OA patients and healthy controls. RAGE -429T/C and 557G/A showed a significant association between OA patients and healthy controls (P = 0.016 and 0.047, respectively). In haplotype analyses, no RAGE and MMP-1 haplotypes showed associations with OA. Our results suggest that the investigated polymorphism in the RAGE gene play a role in OA in the Han Chinese population. |
| e-ISSN |
16765680 |
| Journal |
Genetics and Molecular Research |
| Issue Number |
3 |
| Volume Number |
14 |
| Language |
English |
| Publisher |
Fundação de Pesquisas Científicas de Ribeirão Preto |
| Publisher Date |
2015-09-25 |
| Publisher Place |
Brazil |
| Access Restriction |
Open |
| Subject Keyword |
Advanced Glycosylation End Product-specific Receptor Genetics Asian Continental Ancestry Group Ethnic Groups Genetic Predisposition To Disease Osteoarthritis, Knee Polymorphism, Single Nucleotide Severity Of Illness Index Calgranulin A Case-control Studies Genetic Association Studies Haplotypes Matrix Metalloproteinase 1 Research Support, Non-u.s. Gov't Discipline Genetics Discipline Molecular Biology Discipline Bioinformatics |
| Content Type |
Text |
| Resource Type |
Article |
