Expression of p16^{INK 4a} is a biomarker of chondrocyte aging but does not cause osteoarthritis.

ABSTRACT: Cellular senescence drives a functional decline of numerous tissues with aging by limiting regenerative proliferation and/or by producing pro-inflammatory molecules known as the senescence-associated secretory phenotype (SASP). The senescence biomarker p16^{INK 4a} is a potent inhibitor of the cell cycle but is not essential for SASP production. Thus, it is unclear whether p16^{INK 4a} identifies senescence in hyporeplicative cells such as articular chondrocytes and whether p16^{INK 4a} contributes to pathologic characteristics of cartilage aging. To address these questions, we examined the role of p16^{INK 4a} in murine and human models of chondrocyte aging. We observed that p16^{INK 4a} mRNA ex

SUBMITTER: Diekman BO 

PROVIDER: S-EPMC6052464 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature