Open AccessIL‐10 induces MC3T3‐E1 cells differentiation towards osteoblastic fate in murine model
Author(s) -
Xiong Yuan,
Yan Chenchen,
Chen Lang,
Endo Yori,
Sun Yun,
Zhou Wu,
Hu Yiqiang,
Hu Liangcong,
Chen Dong,
Xue Hang,
Mi Bobin,
Liu Guohui
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14832
Subject(s) - osteoblast , luciferase , microbiology and biotechnology , chemistry , in vivo , insulin like growth factor 1 receptor , microrna , bone healing , receptor , growth factor , reporter gene , medicine , endocrinology , biology , in vitro , gene expression , gene , transfection , anatomy , biochemistry
Interleukin‐10 (IL‐10) displays well‐documented anti‐inflammatory effects, but its effects on osteoblast differentiation have not been investigated. In this study, we found IL‐10 negatively regulates microRNA‐7025‐5p (miR‐7025‐5p), the down‐regulation of which enhances osteoblast differentiation. Furthermore, through luciferase reporter assays, we found evidence that insulin‐like growth factor 1 receptor (IGF1R) is a miR‐7025‐5p target gene that positively regulates osteoblast differentiation. In vivo studies indicated that the pre‐injection of IL‐10 leads to increased bone formation, while agomiR‐7025‐5p injection delays fracture healing. Taken together, these results indicate that IL‐10 induces osteoblast differentiation via regulation of the miR‐7025‐5p/IGF1R axis. IL‐10 therefore represents a promising therapeutic strategy to promote fracture healing.