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Loss of Vhl in cartilage accelerated the progression of age-associated and surgically induced murine osteoarthritis.

Abstract：

OBJECTIVE:To investigate the role of Vhl in maintaining the integrity of articular cartilage and in the development of experimental osteoarthritis (OA). METHOD:Histology of articular cartilage and subchondral bone in both Vhl cKO and WT mice were analyzed by histopathology and micro-CT. Articular cartilage destruction and proteoglycan loss were scored in aged (12-month-old) mice as well as in mice with surgically induced OA. Apoptosis of cartilage in age-related and surgically induced OA was detected with TUNEL assay. Expressions of von Hippel-Lindau (VHL), Fas, LC-3, HIF-1α, HIF-2α, p-mTOR and MMP-13 in the knee joints were analyzed by immunostaining. RESULTS:No gross differences in cartilage were observed between Vhl cKO and WT mice at age 4 months. However, Vhl cKO mice displayed accelerated age-associated spontaneous OA and surgically induced OA. Cartilage destruction and proteoglycan loss were observed in the absence of Vhl. In addition, inactivation of Vhl resulted in up-regulation of HIF-2α and increased chondrocyte apoptosis and decreased expression of autophagy during OA development. Immunohistochemical staining also showed that Vhl deficiency led to increased expression of Fas, p-mTOR and MMP-13, and those genes were associated with cell apoptosis, autophagy and cartilage matrix breakdown, respectively. CONCLUSION:Loss of Vhl in adult articular cartilage is associated with earlier dysregulation of cartilage homeostasis, characterized by an increased chondrocyte apoptosis, compromised chondrocyte autophagy, and an accelerated age-related and surgery-induced OA development. These results highlight the novel role of Vhl in maintaining joint homeostasis and OA development.

journal_name

Osteoarthritis Cartilage

journal_title

Osteoarthritis and cartilage

authors

Weng T,Xie Y,Yi L,Huang J,Luo F,Du X,Chen L,Liu C,Chen D,Chen L

doi

10.1016/j.joca.2014.06.031

subject

Has Abstract

pub_date

2014-08-01 00:00:00

pages

1197-205

issue

8

eissn

1063-4584

issn

1522-9653

pii

S1063-4584(14)01154-6

journal_volume

22

pub_type

杂志文章

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