H3K27 Acetylation-driven IGF2BP2 Mutates during the Aging of MSCs, thereby Influencing Osteogenic Differentiation and Bone Aging.

Zimo Zhou, Kai Kang, Heran Wang, Boya Wen, Da Liu

Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China. · pubmed

Paper

Abstract

Aging-related bone loss is closely linked to mesenchymal stem cell (MSC) senescence, but the underlying epigenetic mechanisms remain unclear. Here, the role of histone H3 lysine 27 acetylation (H3K27ac) and its downstream target IGF2BP2 in MSC aging are investigated. Integrated ChIP-seq and RNA-seq analyses revealed diminished H3K27ac levels in aged murine bone marrow-MSCs (BM-MSCs), accompanied by reduced IGF2BP2 expression. Functional studies demonstrated that both knockdown and overexpression of IGF2BP2 mitigated senescence phenotypes in hydrogen peroxide- and etoposide-induced models. The mutation frequency of H65Q, a key point mutation in IGF2BP2, exhibited variations according to age and sex, and enhanced its binding to

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that mutations in IGF2BP2, driven by H3K27 acetylation changes during aging, influence mesenchymal stem cell senescence and osteogenic differentiation. This research addresses epigenetic mechanisms underlying MSC aging, which is directly related to the root causes of aging and age-related bone loss.

Author of this paper? Send a correction.