LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling

Abstract Temporomandibular joint OA (TMJOA) is a common degenerative joint disease, leads to structural damage and ultimately loss of function. Matrix degradation is one of the first pathogenesis during the progression of OA, it was effective to inhibit matrix degradation to block the development of...

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Autores principales:	Caixia Zhang, Mengjiao Zhu, Huijuan Wang, Juan Wen, Ziwei Huang, Sheng Chen, Hongting Zhao, Huang Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/870554d5f4e14b82a5f20a9dfbb74f3d
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spelling	oai:doaj.org-article:870554d5f4e14b82a5f20a9dfbb74f3d2021-12-02T16:34:54ZLOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling10.1038/s41598-021-96348-x2045-2322https://doaj.org/article/870554d5f4e14b82a5f20a9dfbb74f3d2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-96348-xhttps://doaj.org/toc/2045-2322Abstract Temporomandibular joint OA (TMJOA) is a common degenerative joint disease, leads to structural damage and ultimately loss of function. Matrix degradation is one of the first pathogenesis during the progression of OA, it was effective to inhibit matrix degradation to block the development of OA. In this study, an in vivo model (compressive mechanical force) and an in vitro model (IL-1β) were used to induce OA-like changes in TMJ cartilage and chondrocytes. We revealed lysyl oxidase like-2 (LOXL2) play a critical role in TMJOA. LOXL2 expression decreased in mechanical stress/IL-β induced TMJOA-like lesions in both in vivo models and in vitro models. Furthermore, recombinant LOXL2 (rhLOXL2) treatment ameliorated the degenerative changes induced by mechanical stress in vivo, including the thinning cartilage, down-expression of collagen II and proteoglycan, and over-expression of TNF-a, while LOXL2 antibody (anti-LOXL2) treatment exacerbated these changes. Mechanistically, the protection of LOXL2 in chondrocytes was induced partly through activation of the Integrin/FAK pathway. The inhibition of the Integrin/FAK pathway could neutralized the effects caused by rhLOXL2. Collectively, our study suggests that the LOXL2 plays a protective role in mechanical stress induced TMJOA-like changes, and the Integrin/FAK pathway may be a key downstream pathway in this process.Caixia ZhangMengjiao ZhuHuijuan WangJuan WenZiwei HuangSheng ChenHongting ZhaoHuang LiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Caixia Zhang Mengjiao Zhu Huijuan Wang Juan Wen Ziwei Huang Sheng Chen Hongting Zhao Huang Li LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling
description	Abstract Temporomandibular joint OA (TMJOA) is a common degenerative joint disease, leads to structural damage and ultimately loss of function. Matrix degradation is one of the first pathogenesis during the progression of OA, it was effective to inhibit matrix degradation to block the development of OA. In this study, an in vivo model (compressive mechanical force) and an in vitro model (IL-1β) were used to induce OA-like changes in TMJ cartilage and chondrocytes. We revealed lysyl oxidase like-2 (LOXL2) play a critical role in TMJOA. LOXL2 expression decreased in mechanical stress/IL-β induced TMJOA-like lesions in both in vivo models and in vitro models. Furthermore, recombinant LOXL2 (rhLOXL2) treatment ameliorated the degenerative changes induced by mechanical stress in vivo, including the thinning cartilage, down-expression of collagen II and proteoglycan, and over-expression of TNF-a, while LOXL2 antibody (anti-LOXL2) treatment exacerbated these changes. Mechanistically, the protection of LOXL2 in chondrocytes was induced partly through activation of the Integrin/FAK pathway. The inhibition of the Integrin/FAK pathway could neutralized the effects caused by rhLOXL2. Collectively, our study suggests that the LOXL2 plays a protective role in mechanical stress induced TMJOA-like changes, and the Integrin/FAK pathway may be a key downstream pathway in this process.
format	article
author	Caixia Zhang Mengjiao Zhu Huijuan Wang Juan Wen Ziwei Huang Sheng Chen Hongting Zhao Huang Li
author_facet	Caixia Zhang Mengjiao Zhu Huijuan Wang Juan Wen Ziwei Huang Sheng Chen Hongting Zhao Huang Li
author_sort	Caixia Zhang
title	LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling
title_short	LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling
title_full	LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling
title_fullStr	LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling
title_full_unstemmed	LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling
title_sort	loxl2 attenuates osteoarthritis through inactivating integrin/fak signaling
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/870554d5f4e14b82a5f20a9dfbb74f3d
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LOXL2 attenuates osteoarthritis through inactivating Integrin/FAK signaling

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