p21 deficiency is susceptible to osteoarthritis through STAT3 phosphorylation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-12

AUTHORS

Shinya Hayashi, Takaaki Fujishiro, Shingo Hashimoto, Noriyuki Kanzaki, Nobuaki Chinzei, Shinsuke Kihara, Koji Takayama, Tomoyuki Matsumoto, Kotaro Nishida, Masahiro Kurosaka, Ryosuke Kuroda

ABSTRACT

INTRODUCTION: Osteoarthritis (OA) is a multifactorial disease, and recent studies have suggested that cell cycle-related proteins play a role in OA pathology. p21 was initially identified as a potent inhibitor of cell cycle progression. However, it has been proposed that p21 is a regulator of transcription factor activity. In this study, we evaluated the role of p21 in response to biomechanical stress. METHODS: Human chondrocytes were treated with p21-specific small interfering RNA (siRNA), and cyclic tensile strain was introduced in the presence or absence of a signal transducer and activator of transcription 3 (STAT3)-specific inhibitor. Further, we developed an in vivo OA model in a p21-knockout background for in vivo experiments. RESULTS: The expression of matrix metalloproteinase (MMP13) mRNA increased in response to cyclic tensile strain following transfection with p21 siRNA, whereas the expression of aggrecan was decreased. Phospho-STAT3 and MMP-13 protein levels increased following downregulation of p21, and this was reversed by treatment with a STAT3 inhibitor. p21-deficient mice were susceptible to OA, and this was associated with increased STAT3 phosphorylation, elevated MMP-13 expression, and elevation of synovial inflammation. The expression of p21 mRNA was decreased and phosphorylation of STAT3 was elevated in human OA chondrocytes. CONCLUSIONS: The lack of p21 has catabolic effects by regulation of aggrecan and MMP-13 expression through STAT3 phosphorylation in the cartilage tissue. p21 may function as a regulator of transcriptional factors other than the inhibitor of cell cycle progression in the cartilage tissue. Thus, the regulation of p21 may be a therapeutic strategy for the treatment of OA. More... »

PAGES

314

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13075-015-0828-6

DOI

http://dx.doi.org/10.1186/s13075-015-0828-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1017313489

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26546411


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