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• W1991164035 abstract "Purpose: Osteoarthritis is one of the most common chronic musculoskeletal disorders and a cause of serious morbidity and disablement, particularly in the elderly population. The disease can be confined to one or more joints, but can also be generalized. Progressive damage to the articular cartilage and bone leads to pain and loss of joint function. The current therapeutic strategies are limited: changes in lifestyle and appropriate exercise and use of painkillers and anti-inflammatory medication. Eventually, in many cases, joint replacement surgery may be required, especially for the larger joints. The development of osteoarthritis is very complex, due to the activation of several signaling pathways in the different tissues composing the joint, and is influenced by both genetic and acquired or environmental risk factors. We have recently described an association between polymorphisms in the ANP32a gene and osteoarthritis. Anp32a (acidic leucine-rich nuclear phosphoprotein 32 family member a) functions as a tumor suppressor gene and a regulator of gene transcription. It is also implicated in the stabilization of RNA, intracellular transport and apoptosis. Moreover, Anp32a associates with Axin-1 and Phosphatase 2A, molecules that exert a regulating role in the Wingless-type signaling (Wnt) pathway. Wnts are key players in embryonic development with effects on cell differentiation, proliferation and migration. Wnt signaling is also critical for the induction as well as the maintenance of skeletal tissues, is involved in the very early stages of joint formation and appears to be re-activated during adult joint homeostasis. Methods: Different established mouse models for osteoarthritis (OA) were introduced in Anp32a knockout mice. These include papain-induced arthritis, which is characterized by direct cartilage proteoglycan loss, and DMM-induced arthritis, which is a surgical model of meniscus destabilization, leading to uni-compartimental arthritis, caused by mild instability of the knee. Severe instability of the knee was caused by affecting collagen-rich structures in a collagenase-induced arthritis model. A last model mimics Il1-driven inflammatory arthritis. A transcriptome analysis to study molecular changes in the articular cartilage of mice deficient in Anp32a was also performed. RNA was isolated from articular cartilage of the tibial plateau of knees and used in a microarray study to compare gene expression with cartilage from normal wildtype C57Bl/6 mice. Four C57Bl/6 wild type (WT) and 4 Anp32a-/- mice RNA samples were analyzed on Affymetrix Mouse 430 2.0 chips. Results: In the DMM- and collagenase-induced OA models, absence of Anp32a resulted in increased cartilage damage, contributing to the development of osteoarthritis. In the papain-induced OA model, a trend for increased cartilage damage was observed in the Anp32a-/- mice. Induction of the mBSA OA model in the Anp32a-/- mice lead to increased inflammation and bone erosion. Several genes related to chondrogenesis, to the development of OA and to the Wnt signaling pathway were identified in our transcriptome analysis. Conclusions: Our analysis provides evidence for an important role for Anp32a in joint homeostasis and highlights the complex biology of Wnt signaling in the joint." @default.
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• W1991164035 date "2015-04-01" @default.
• W1991164035 modified "2023-09-30" @default.
• W1991164035 title "Loss of ANP32a increases severity of osteoarthritis in different mouse models" @default.
• W1991164035 doi "https://doi.org/10.1016/j.joca.2015.02.861" @default.
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