Dataset of "Mitochondria from osteolineage cells regulate myeloid cells mediated bone resorption"

Interaction between osteolineage cells and myeloid cells plays important roles in maintaining skeletal homeostasis. Herein, we found that osteolineage cells transfer mitochondria to myeloid cells. Impair the transfer of mitochondria by deleting Miro1 in osteolineage cells led to the increased myeloid cell commitments towards osteoclastic lineage cells and promoted bone resorption. In detail, impaired mitochondria transfer from osteolineage cells altered the glutathione (GSH) metabolism and protecting osteoclastic lineage cells from ferroptosis, thus promoting osteoclast activities. Further, mitochondria transfer from osteolineage cells to myeloid cells also involved in the regulation of glucocorticoid-induced osteoporosis (GIOP), and GSH depletion alleviated the progression of GIOP. These findings revealed an unappreciated mechanism underlying the interaction between osteolineage cells and myeloid cells to regulate skeletal metabolic homeostasis and provide new insights of GIOP progression.

成骨系细胞（osteolineage cells）与髓系细胞（myeloid cells）之间的相互作用在维持骨骼稳态中发挥重要作用。本研究发现，成骨系细胞可将线粒体转移至髓系细胞。通过敲除成骨系细胞中的Miro1以损伤线粒体转移后，髓系细胞向破骨细胞系的分化倾向增强，并促进了骨吸收。具体而言，成骨系细胞的线粒体转移受损会改变谷胱甘肽（glutathione, GSH）代谢，使破骨细胞系免于铁死亡，进而增强破骨细胞的活性。进一步研究表明，成骨系细胞向髓系细胞的线粒体转移还参与调控糖皮质激素诱导性骨质疏松症（glucocorticoid-induced osteoporosis, GIOP），而谷胱甘肽耗竭可缓解GIOP的疾病进展。本研究揭示了成骨系细胞与髓系细胞相互作用调控骨骼代谢稳态的一种未被认知的机制，同时为GIOP的疾病进展提供了新的研究思路。