Insulin-like Growth Factor 2 mRNA-binding Protein 2 Regulates PINK1 Expression through m

Yu Ji, Yajun Cui, Lingshuang Li, Tianyu Cao, Hongrui Liu, Minqi Li

Department of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Jinan, China; Center of Osteoporosis and Bone Mineral Research, Shandong University, Jinan, China.Department of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Jinan, China; Center of Osteoporosis and Bone Mineral Research, Shandong University, Jinan, China. · pubmed

Paper

Abstract

The senescence and altered differentiation potential of bone marrow mesenchymal stem cells (BMSCs) contribute to the pathogenesis of postmenopausal osteoporosis (PMOP). Insulin-like growth factor 2 mRNA-binding protein (IMP2) has been demonstrated to regulate BMSCs. However, its specific mechanistic actions remain unclear, particularly due to the lack of concrete evidence within the ovariectomy (OVX) in vivo microenvironment. In this study, we utilized Cre-LoxP technology to achieve BMSC-specific IMP2 knockout. This approach conclusively demonstrated in vivo that IMP2 deficiency induces BMSC senescence, suppresses osteogenic differentiation capacity, and leads to significant bone mass reduction in mice. Under OVX conditions, IMP2 knockout also aggravates bone loss. Mechanistically, we argued that IMP2 stabilizes PINK1 mRNA via the N6-methyladenosine (m

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Research summary

The paper claims that IMP2 deficiency induces BMSC senescence and suppresses osteogenic differentiation, leading to bone mass reduction. The study addresses mechanisms related to cellular senescence and differentiation, which are fundamental aspects of aging and age-related diseases.

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