National Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China.
J Nanobiotechnology. 2024 Jun 23;22(1):361. doi: 10.1186/s12951-024-02640-z.
Recently, environmental temperature has been shown to regulate bone homeostasis. However, the mechanisms by which cold exposure affects bone mass remain unclear. In our present study, we observed that exposure to cold temperature (CT) decreased bone mass and quality in mice. Furthermore, a transplant of exosomes derived from the plasma of mice exposed to cold temperature (CT-EXO) can also impair the osteogenic differentiation of BMSCs and decrease bone mass by inhibiting autophagic activity. Rapamycin, a potent inducer of autophagy, can reverse cold exposure or CT-EXO-induced bone loss. Microarray sequencing revealed that cold exposure increases the miR-25-3p level in CT-EXO. Mechanistic studies showed that miR-25-3p can inhibit the osteogenic differentiation and autophagic activity of BMSCs. It is shown that inhibition of exosomes release or downregulation of miR-25-3p level can suppress CT-induced bone loss. This study identifies that CT-EXO mediates CT-induced osteoporotic effects through miR-25-3p by inhibiting autophagy via targeting SATB2, presenting a novel mechanism underlying the effect of cold temperature on bone mass.
最近，环境温度被证明可以调节骨稳态。然而，寒冷暴露影响骨量的机制尚不清楚。在本研究中，我们观察到，暴露于寒冷温度（CT）会减少小鼠的骨量和质量。此外，来自暴露于寒冷温度的小鼠血浆的外泌体（CT-EXO）的移植也可以通过抑制自噬活性来损害 BMSCs 的成骨分化并减少骨量。雷帕霉素是一种有效的自噬诱导剂，可以逆转冷暴露或 CT-EXO 引起的骨丢失。微阵列测序显示，寒冷暴露会增加 CT-EXO 中的 miR-25-3p 水平。机制研究表明，miR-25-3p 可以抑制 BMSCs 的成骨分化和自噬活性。研究表明，抑制外泌体释放或下调 miR-25-3p 水平可以抑制 CT 引起的骨丢失。这项研究表明，CT-EXO 通过靶向 SATB2 抑制自噬来介导 CT 诱导的骨质疏松效应，通过 miR-25-3p 抑制自噬，从而为冷温度对骨量的影响提供了一种新的机制。
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