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자료유형
학술저널
저자정보
Seo Jin Hong (Seoul National University) Suhan Jung (School of Dentistry Seoul National University) Ji Sun Jang (School of Dentistry Seoul National University) Shenzheng Mo (School of Dentistry Seoul National University) 권준오 (서울대학교) 김민경 (서울대학교) Hong-Hee Kim (Seoul National University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제45권 제10호
발행연도
2022.10
수록면
749 - 760 (12page)

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Osteoclast generation from monocyte/macrophage lineage precursor cells needs to be tightly regulated to maintain bone homeostasis and is frequently over-activated in inflammatory conditions. PARK2, a protein associated with Parkinson’s disease, plays an important role in mitophagy via its ubiquitin ligase function. In this study, we investigated whether PARK2 is involved in osteoclastogenesis. PARK2 expression was found to be increased during the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation. PARK2 gene silencing with siRNA significantly reduced osteoclastogenesis induced by RANKL, LPS (lipopolysaccharide), TNFα (tumor necrosis factor α), and IL-1β (interleukin-1β). On the other hand, overexpression of PARK2 promoted osteoclastogenesis. This regulation of osteoclastogenesis by PARK2 was mediated by IKK (inhibitory κB kinase) and NF-κB activation while MAPK (mitogen-activated protein kinases) activation was not involved. Additionally, administration of PARK2 siRNA significantly reduced osteoclastogenesis and bone loss in an in vivo model of inflammatory bone erosion. Taken together, this study establishes a novel role for PARK2 as a positive regulator in osteoclast differentiation and inflammatory bone destruction.

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