Yang Yi, Zhang Ning, Wang Shan, Wen Ya
Department of Neurology, The Second Hospital of Hebei Medical University, Hebei Key Laboratory for Neurology, Hebei, 050000, China.
Department of Neurology, The Second Hospital of Hebei Medical University, Hebei, 050000, China.
Curr Neurovasc Res. 2018;15(2):103-110. doi: 10.2174/1567202615666180601081409.
Our previous work has indicated that miR-155 expression induces inflammatory responses in ischemic cerebral tissues. However, the delicate regulation of miR-155-modifed inflammatory responses has remained enigmatic. In the present study, we found that autophagy is induced by ischemia through miR-155 and involved in neural injury. Subsequently, miR-155- induced autophagy modifies inflammatory responses through regulating TLR4/NF-κB pathway in ischemic cerebral tissues. Thus, miR-155 elevated autophagy is detrimental for ischemic cerebral injury and miR-155-induced autophagy modulates inflammatory responses through activating TLR4/NF-κB pathway.
我们之前的研究表明,miR-155的表达可诱导缺血性脑组织中的炎症反应。然而,miR-155修饰的炎症反应的精细调控机制仍不清楚。在本研究中,我们发现缺血通过miR-155诱导自噬并参与神经损伤。随后,miR-155诱导的自噬通过调节缺血性脑组织中的TLR4/NF-κB通路来修饰炎症反应。因此,miR-155升高的自噬对缺血性脑损伤有害,且miR-155诱导的自噬通过激活TLR4/NF-κB通路来调节炎症反应。