NDLI: c-Jun transactivates Puma gene expression to promote osteoarthritis.

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c-Jun transactivates Puma gene expression to promote osteoarthritis.

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c-Jun transactivates Puma gene expression to promote osteoarthritis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lu, Huading Hou, Gang Dai, Yuhu Zhang, Yongkai Zhao, Huiqing
Description	Author Affiliation: Lu H ( Department of Orthopaedics, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, P.R. China.); Hou G ( Department of Orthopaedics, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, P.R. China.); Zhang Y ( Department of Orthopaedics, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, P.R. China.); Dai Y ( Department of Orthopaedics, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, P.R. China.); Zhao H ( Department of Orthopaedics, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, P.R. China.)
Abstract	Osteoarthritis (OA) is a chronic degenerative joint disorder in which genetic, hormonal, mechanical and ageing factors affect its progression. Current studies are focusing on chondrocytes as a key mediator of OA at a cellular level. however, the mechanism underlying chondrocyte apoptosis remains unclear. PUMA is a pro-apoptotic member of the BH3-only subgroup of the Bcl-2 family and is involved in a large number of physiological and pathological processes. In the present study, we examined whether PUMA has a role in IL-1ß-induced apoptosis and whether the c-Jun N-terminal kinase (JNK)/c-Jun pathway mediates the induction of PUMA, thus contributing to chondrocyte apoptosis. The results demonstrated an increase in PUMA protein and mRNA levels in cultured mouse chondrocytes following 4 h of IL-1ß treatment. Furthermore, this upregulation of PUMA was critical for chondrocyte apoptosis as knockdown of PUMA using PUMA-specific siRNA significantly reduced apoptosis in cultured cells. Upon pharmacological inhibition of the JNK/c-Jun pathway with CE11004 or SP600125, the expression of PUMA was notably suppressed with a concomitant decrease in apoptosis observed in IL-1ß-treated chondrocytes. Also, immunohistochemical studies revealed that the PUMA and c-Jun proteins were upregulated in chondrocytes from the articular cartilage of OA patients. Together, these data suggest a role for PUMA and the JNK/c-Jun pathway in the regulation of chondrocyte apoptosis during OA.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	9
Language	English
Publisher	Spandidos Publications
Publisher Date	2014-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Apoptosis Regulatory Proteins Genetics Gene Expression Regulation Osteoarthritis Metabolism Proto-oncogene Proteins C-jun Tumor Suppressor Proteins Animals Apoptosis Drug Effects Cells, Cultured Chondrocytes Disease Models, Animal Interleukin-1beta Pharmacology Jnk Mitogen-activated Protein Kinases Mice Rna, Messenger Signal Transduction Up-regulation Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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