ADAMTS5−/− mice have less subchondral bone changes after induction of osteoarthritis through surgical instability: implications for a link between cartilage and subchondral bone changes

Botter, Sander M.; Glasson, S.S.; Hopkins, Bei; Clockaerts, S.; Weinans, Harrie; Leeuwen, Johannes P.T.M. van; Osch, Gerjo J. V. M. van

doi:10.1016/j.joca.2008.09.018

Cited by 115 publications

(103 citation statements)

References 67 publications

(51 reference statements)

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“…At 8 weeks of age, 10 mice per group were anesthetized and instability of the right knee joint was induced by transection of the anterior attachment of the medial meniscus to the tibial plateau. Left knee joints were left intact and are termed “left unoperated control joints” (Botter et al., 2009; Glasson, Blanchet & Morris, 2007). For each intra‐articular administration of DAPT in miR‐146a −/− mice (Hosaka et al., 2013), we injected 5 μl of 5 μ m DAPT solution, which was prepared by diluting 50 m m DAPT in dimethyl sulfoxide (DMSO) with injectable normal saline at 1:10,000, and 10 μl of DMSO diluted with normal saline (1:10,000) as the control.…”

Section: Methodsmentioning

confidence: 99%

Evidence that miR‐146a attenuates aging‐ and trauma‐induced osteoarthritis by inhibiting Notch1, IL‐6, and IL‐1 mediated catabolism

Guan

Yang

et al. 2018

Aging Cell

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SummaryPrimary osteoarthritis (OA) is associated with aging, while post‐traumatic OA (PTOA) is associated with mechanical injury and inflammation. It is not clear whether the two types of osteoarthritis share common mechanisms. We found that miR‐146a, a microRNA‐associated with inflammation, is activated by cyclic load in the physiological range but suppressed by mechanical overload in human articular chondrocytes. Furthermore, miR‐146a expression is decreased in the OA lesions of human articular cartilage. To understand the role of miR‐146a in osteoarthritis, we systemically characterized mice in which miR‐146a is either deficient in whole body or overexpressed in chondrogenic cells specifically. miR‐146a‐deficient mice develop early onset of OA characterized by cartilage degeneration, synovitis, and osteophytes. Conversely, miR‐146a chondrogenic overexpressing mice are resistant to aging‐associated OA. Loss of miR‐146a exacerbates articular cartilage degeneration during PTOA, while chondrogenic overexpression of miR‐146a inhibits PTOA. Thus, miR‐146a inhibits both OA and PTOA in mice, suggesting a common protective mechanism initiated by miR‐146a. miR‐146a suppresses IL‐1β of catabolic factors, and we provide evidence that miR‐146a directly inhibits Notch1 expression. Therefore, such inhibition of Notch1 may explain suppression of inflammatory mediators by miR‐146a. Chondrogenic overexpression of miR‐146a or intra‐articular administration of a Notch1 inhibitor alleviates IL‐1β‐induced catabolism and rescues joint degeneration in miR‐146a‐deficient mice, suggesting that miR‐146a is sufficient to protect OA pathogenesis by inhibiting Notch signaling in the joint. Thus, miR‐146a may be used to counter both aging‐associated OA and mechanical injury‐/inflammation‐induced PTOA.

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Section: Methodsmentioning

confidence: 99%

Evidence that miR‐146a attenuates aging‐ and trauma‐induced osteoarthritis by inhibiting Notch1, IL‐6, and IL‐1 mediated catabolism

Guan

Yang

et al. 2018

Aging Cell

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“…Several animal studies showed that an initial thinning of the subchondral bone plate [19,20] is followed by a recovery phase leading to subsequent thickening of the subchondral plate due to enhanced osteoblast activity [20][21][22]. During this un-physiological high bone turnover in OA joints, there is an altered phenotypic expression of osteoblasts, which results in the production of sclerotic bone together with cyst formation and osteophyte development [4,9,23].…”

Section: Introductionmentioning

confidence: 99%

Inhibited osteoclastic bone resorption through alendronate treatment in rats reduces severe osteoarthritis progression

Siebelt

Waarsing

Groen

et al. 2014

Bone

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“…Recent advances in animal OA model have allowed us to quantify molecular changes of OA over time [8,9]. Postn is a vitamin K-dependent glutamate-containing matri-cellular protein, originally isolated from a mouse osteoblast cell [5].…”

Section: Discussionmentioning

confidence: 99%

Elevated Expression of Periostin in Cartilage in Early Experimental Osteoarthritis

Zhang¹

2017

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Osteoarthritis (OA) is characterized by the degeneration of affected joints leading to pain and reduced mobility.Periostin appears as a potential candidate in transducing mechanical signals to stimulate chondrocyte proliferation. 15 rats (E-group) underwent both medial meniscectomy and medial collateral ligament (MCL) transaction, while the other 15 rats (S-group) underwent sham surgery. Animals were killed at 1, 2, and 4 weeks postsurgery, and 5 animals were put into use per-time point in each treatment group. Cartilage was harvested from tibial plateau and femoral condyle. We examined the level of Postn expression in cartilage of the experimental OA, using real-time PCR and immunohistochemistry analysis. The expression of Postn was about 2-fold higher at 1 week (P=0.08<0.05), 4-fold higher at 2 weeks (P=0.003<0.05) and 4-fold higher at 4 weeks (P=0.034<0.05) post-surgery in E-group compared to S-group. Postn protein expression levels were markedly increased in the E-Group compared with the S-Group at 1, 2 and 4 weeks post-surgery. This study will be of benefit to those subsequent studies using the OA model to evaluate the outcomes of Postn epxpression in mechanism of OA. Postn may play prominent roles in pathogenic mechanisms of OA.

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ADAMTS5−/− mice have less subchondral bone changes after induction of osteoarthritis through surgical instability: implications for a link between cartilage and subchondral bone changes

Cited by 115 publications

References 67 publications

Evidence that miR‐146a attenuates aging‐ and trauma‐induced osteoarthritis by inhibiting Notch1, IL‐6, and IL‐1 mediated catabolism

Evidence that miR‐146a attenuates aging‐ and trauma‐induced osteoarthritis by inhibiting Notch1, IL‐6, and IL‐1 mediated catabolism

Inhibited osteoclastic bone resorption through alendronate treatment in rats reduces severe osteoarthritis progression

Elevated Expression of Periostin in Cartilage in Early Experimental Osteoarthritis

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