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- Title
Aged bone matrix-derived extracellular vesicles as a messenger for calcification paradox.
- Authors
Wang, Zhen-Xing; Luo, Zhong-Wei; Li, Fu-Xing-Zi; Cao, Jia; Rao, Shan-Shan; Liu, Yi-Wei; Wang, Yi-Yi; Zhu, Guo-Qiang; Gong, Jiang-Shan; Zou, Jing-Tao; Wang, Qiang; Tan, Yi-Juan; Zhang, Yan; Hu, Yin; Li, You-You; Yin, Hao; Wang, Xiao-Kai; He, Ze-Hui; Ren, Lu; Liu, Zheng-Zhao
- Abstract
Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called "calcification paradox". Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861. This study uncovers the role of extracellular vesicles from bone matrix as a messenger in the development of osteoporosis and vascular calcification (calcification paradox) during skeletal aging and menopause by transferring miR-483-5p and miR-2861.
- Subjects
EXTRACELLULAR vesicles; CALCIFICATION; ARTERIAL calcification; VASCULAR smooth muscle; CLIMACTERIC; BONE resorption; VESICLES (Cytology)
- Publication
Nature Communications, 2022, Vol 13, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-022-29191-x