Activin A rescues preterm brain injury through a novel Noggin/BMP4/Id2 signaling pathway
| Autor: | Xiaojuan, Su, Junjie, Ying, Dongqiong, Xiao, Xia, Qiu, Shiping, Li, Fengyan, Zhao, Jun, Tang |
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| Rok vydání: | 2022 |
| Předmět: | |
| Zdroj: | International Journal of Molecular Medicine. 51 |
| ISSN: | 1791-244X 1107-3756 |
| Popis: | Activin A (Act A) has been reported to promote oligodendrocyte progenitor cell (OPC) differentiation in vitro and improve neurological outcomes in adult mice. However, the roles and mechanisms of action of Act A in preterm brain injury are unknown. In the present study, P5 rats were subjected to hypoxia‑ischemia to establish a neonatal white matter injury (WMI) model and Act A was injected via the lateral ventricle. Pathological characteristics, OPC differentiation, myelination, and neurological performance were analyzed. Further, the involvement of the Noggin/BMP4/Id2 signaling pathway in the roles of Act A in WMI was explored. Act A attenuated pathological damage, promoted OPC differentiation, enhanced myelin sheath and myelinated axon formation, and improved neurological performance of WMI rats. Moreover, Act A enhanced noggin expression, which, in turn, inhibited the expression of bone morphogenetic protein 4 (BMP4) and inhibitor of DNA binding 2 (Id2). Furthermore, upregulation of Id2 completely abolished the rescue effects of Act A in WMI rats. In conclusion, the present findings suggested that Act A rescues preterm brain injury via targeting a novel Noggin/BMP4/Id2 signaling pathway. |
| Databáze: | OpenAIRE |
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