细胞生物学
神经酰胺
信号转导
细胞外
细胞内
信使核糖核酸
细胞信号
微泡
生物
脂肪组织
化学
基因表达
体内
酶
细胞
免疫系统
脂质信号
表型
酸性鞘磷脂酶
外体
鞘磷脂
第二信使系统
基因表达调控
细胞外小泡
鞘脂
下调和上调
荧光素酶
作者
Clair Crewe,Christy Gliniak,Toshiharu Onodera,S Chen,Jan‐Bernd Funcke,May-Yun Wang,Snigdha Tiash,Yun-Ling Pai,Marjori Russo,Saket Awadhesbhai Patel,Ze Yu,Yi-Cian Zheng,Alex Larkin,Chao Xing,Laurent Gautron,Chun‐Kan Chen,Chen Liu,Philipp E. Scherer
标识
DOI:10.1038/s41467-026-71740-1
摘要
Extracellular vesicles (EVs) are nano-sized, membrane-delimited, particles released by cells that carry signaling macromolecules. A major pathway of EV production is potentiated by neutral sphingomyelinase 2 (SMPD3/nSMAse2), an enzyme that generates ceramide from sphingomyelin. In our attempt to study this pathway in adipocytes of male mice, we discover that the elimination of SMPD3 from adipocytes in vivo triggers a signal to surrounding immune cell-like preadipocytes to release EVs that carry SMPD3 mRNA. This results in a widespread increase in SMPD3 mRNA in purified null adipocytes without a change in the transcripts of other enzymes involved in ceramide metabolism. These results point to a selective mechanism by which specific mRNA molecules are acquired from the microenvironment to a level that can restore expression of mRNA and protein in a cell that is depleted of the corresponding genetic information. Extracellular vesicles (EVs) mediate intercellular communication by transferring signaling macromolecules. Unexpectedly, the author here identifies that adipocyte-specific loss of SMPD3 triggers neighboring preadipocytes to release EVs containing SMPD3 mRNA, restoring SMPD3 expression in genetically null adipocytes.
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