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Targeted inhibition of ATP5B gene prevents bone erosion in collagen-induced arthritis by inhibiting osteoclastogenesis.
Southern Medical University, Guangzhou, China.
Southern Medical University, Guangzhou, China.
Southern Medical University, Guangzhou, China.
Southern Medical University, Guangzhou, China.
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2021 (English)In: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 165, article id 105458Article in journal (Refereed) Published
Abstract [en]

Bone resorption by osteoclasts is an energy consuming activity, which depends on mitochondrial ATP. ATP5B, a mitochondrial ATP synthase beta subunit, is a catalytic core involved in producing ATP. Here, we investigated the contribution of ATP5B in osteoclast differentiation and joint destruction. ATP5B (LV-ATP5B) targeting or non-targeting (LV-NC) siRNA containing lentivirus particles were transduced into bone marrow macrophage derived osteoclasts or locally administered to arthritic mouse joints. Inhibition of ATP5B reduced the expression of osteoclast related genes and proteins, suppressed bone resorption by significantly impairing F-actin formation and decreased the levels of adhesion-associated proteins. In addition, ATP5B deficiency caused osteoclast mitochondrial dysfunction and, impaired the secretion of vacuole protons and MMP9. Importantly, inhibition of ATP5B expression, protected arthritis mice from joint destructions although serum levels of inflammatory mediators (TNF-α, IL-1β) and IgG2α antibodies were unaffected. These results demonstrate an essential function of ATP5B in osteoclast differentiation and bone resorption, and suggest it as a potential therapeutic target for protecting bones in RA.

Place, publisher, year, edition, pages
2021. Vol. 165, article id 105458
Keywords [en]
ATP5B, CIA, Mitochondrial metabolism, Osteoclasts
National Category
Medical Genetics
Identifiers
URN: urn:nbn:se:hh:diva-48321DOI: 10.1016/j.phrs.2021.105458PubMedID: 33515708OAI: oai:DiVA.org:hh-48321DiVA, id: diva2:1702427
Available from: 2022-10-10 Created: 2022-10-10 Last updated: 2023-02-22Bibliographically approved

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Nandakumar, Kutty Selva

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