Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (46): 8575-8582.doi: 10.3969/j.issn.2095-4344.2012.46.006

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A mitochondrial PCR gene chip based study on the pathogenesis of osteoarthritis

Pan Jian-ying, Shen Jun, Zhang Rong-kai, Li Zhi-fu, Cai Dao-zhang   

  1. Department of Bone and Joint Surgery, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
  • Received:2012-08-08 Revised:2012-10-15 Online:2012-11-11 Published:2013-03-16
  • Contact: Cai Dao-zhang, Doctor, Doctoral supervisor, Professor, Chief physician, Department of Bone and Joint Surgery, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China daozhangcai@medmail.com
  • About author:Pan Jian-ying★, Master, Physician, Department of Bone and Joint Surgery, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China storm0132002@163.com

Abstract:

BACKGROUND: Chondrocytes play a significant role in repairing damaged cartilage tissue as well as in maintaining the integrity of the cartilage. Mitochondria are involved in a large amount of biochemical processes, and mitochondrial impairment has a closed relationship with cell apoptosis, senescence and pathological process of osteoarthritis.
OBJECTIVE: To detect the differential expression of mitochondrial genes by using gene chip based mitochondrial gene analyses.
METHODS: Articular chondrocytes were collected from healthy people and osteoarthritis patients, then extracted and cultured followed by RNA isolation and quality assessment, mRNA isolation and strand cDNA synthesis. After all, real-time quantitative PCR was performed.
RESULTS AND CONCLUSION: Among 84 mitochondrial genes, 18 genes were unambiguously identified as significantly altered in osteoarthritis: 15 of them (BBC3, BCL2, SLC25A37, etc.) were up-regulated at both fold changes and fold regulation > 2, and three of them (CPT1B, SLC25A16, SLC25A24) were down-regulated at fold change < 0.5 and fold regulation < 2. The grouping of 18 functional genes is as follows: membrane polarization & potential: BCL2, BCL2L1, TP53, UCP1, UCP3; mitochondrial transport: BCL2, BCL2L1, CPT1B, FXC1 (TIMM10B), MFN2, STARD3, TP53, UCP1, UCP3; small molecule transport: SLC25A16, SLC25A2, SLC25A24, SLC25A31, SLC25A37; targeting proteins to mitochondria: FXC1 (TIMM10B), MFN2; mitochondrion protein import: COX18, FXC1 (TIMM10B); inner membrane translocation: FXC1 (TIMM10B), TIMM17B; mitochondrial fission & fusion: COX18, MFN2; mitochondrial localization: MFN2; apoptotic genes: BBC3, BCL2, BCL2L1, SOD2, P53. These findings indicate that mitochondrial energy metabolism dysfunction occurs obviously in osteoarthritis chondrocytes.

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