miRNA-144 induces microglial autophagy and inflammation following intracerebral hemorrhage

التفاصيل البيبلوغرافية
العنوان: miRNA-144 induces microglial autophagy and inflammation following intracerebral hemorrhage
المؤلفون: Peng Ye, Zhao Yang, Haizhen Duan, Tianxi Zhang, Anyong Yu, Juan Wang, Song Wang, Shanchuan Zhong, Wenyi Zhong
المصدر: Immunology letters. 182
سنة النشر: 2016
مصطلحات موضوعية: 0301 basic medicine, Immunology, Regulator, Gene Expression, Inflammation, Biology, 03 medical and health sciences, Mice, Downregulation and upregulation, microRNA, Gene expression, medicine, Autophagy, Immunology and Allergy, Animals, cardiovascular diseases, PI3K/AKT/mTOR pathway, Cerebral Hemorrhage, Microglia, TOR Serine-Threonine Kinases, nervous system diseases, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Cancer research, medicine.symptom
الوصف: Autophagic activation mediated inflammation contributes to brain injury of intracerebral hemorrhage (ICH). MiRNAs play a key role in inflammation, which negatively and posttranscriptionally regulate gene expression and function. Modulating the mTOR signal, a central regulator of autophagy, could be of great significance for ICH. However, the specific of miRNA is unknown. In the current study, we detected the miRNA-144 expression, autophagic activity and inflammation of microglia in ICH. We also knocked down endogenous miRNA-144 to regulate autophagy and inflammation in ICH. In addition, we assessed the neurological damge in ICH mice. We found that ICH promoted miRNA-144 expression but downregulated mTOR expression. In addition, upregulation of mTOR attenuated microglial autophagy and inflammation in ICH. Furthermore, downregulation of miRNA-144 also inhibited inflammation, brain edema and improved neurological functions in ICH mice. Taken together, our findings suggested that miRNA-144 was a crucial regulator of autophagy via regulation of mTOR, and represented a promising therapeutical strategy for ICH.
تدمد: 1879-0542
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d8f54ab23a7f5c54338fcba5a3537f4c
https://pubmed.ncbi.nlm.nih.gov/28062218
حقوق: CLOSED
رقم الأكسشن: edsair.doi.dedup.....d8f54ab23a7f5c54338fcba5a3537f4c
قاعدة البيانات: OpenAIRE