ORC ID , Chong-Jie Cheng1, Jian-Jun Zhong1, Jun-Chi He1, Zhao-Si Zhang1, Zhi-Gang Wang1, Xiao-Chuan Sun1, Han Liu PhD 2 ORC ID ">
  • Users Online: 1103
  • Home
  • Print this page
  • Email this page
RESEARCH ARTICLE
Year : 2022  |  Volume : 17  |  Issue : 8  |  Page : 1776-1784

Essential role of MALAT1 in reducing traumatic brain injury


1 Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
2 Department of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing; Department of Neurosurgery, Qilu Hospital of Shandong University (Qingdao Campus), Qingdao, Shandong Province, China

Correspondence Address:
Han Liu
Department of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing; Department of Neurosurgery, Qilu Hospital of Shandong University (Qingdao Campus), Qingdao, Shandong Province
China
Login to access the Email id

Source of Support: The study was supported by the National Natural Science Foundation of China, No. 81571159 (to XCS); the National Natural Science Foundation of China (Youth Program), No. 81601072 (to CJC); and the Natural Science Foundation of Chongqing, China, No. cstc2019jcyj-msxmX0830 (to CJC), Conflict of Interest: None


DOI: 10.4103/1673-5374.332156

Rights and Permissions

As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration. In MALAT1-deficient mice, endothelial cell proliferation in the injured cortex, functional vessel density and cerebral blood flow were reduced. Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2 (EZH2) as a downstream factor of MALAT1 in endothelial cells. Jagged-1, the Notch homolog 1 (NOTCH1) agonist, reversed the MALAT1 deficiency-mediated impairment of angiogenesis. Taken together, our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed136    
    Printed2    
    Emailed0    
    PDF Downloaded20    
    Comments [Add]    

Recommend this journal