miR-140-5p Attenuates Neuroinflammation and Brain Injury in Rats Following Intracerebral Hemorrhage by Targeting TLR4

Inflammation
Shunda WangHeng Gao

Abstract

The Toll-like receptor 4 (TLR4)-mediated neuroinflammation plays a key role in inducing secondary brain injury after intracerebral hemorrhage (ICH). However, how TLR4 is regulated during this pathological process is not well understood. In the present study, by taking advantage of a rat ICH model, we show that miR-140-5p is reversely correlated with TLR4 expression in the peri-hematomal striatum following ICH. In vitro, miR-140-5p directly targets TLR4 and suppresses its expression in a rat neuronal PC12 cell line. Moreover, an intracerebral ventricular injection of miR-140-5p mimics improves neurological function and reduces apoptotic cell death and limits the production of inflammatory cytokines following ICH, indicating that miR-140-5p attenuates brain injury and neuroinflammation in vivo. Furthermore, miR-140-5p suppresses TLR4 expression and inhibits the downstream MyD88/TRIF inflammatory pathway and NF-κB activity following ICH, suggesting that the inhibition of TLR4-mediated neuroinflammation at least in part accounts for the neuroprotective role of miR-140-5 against ICH-induced brain injury in rats. Collectively, these results identify miR-140-5 as a negative regulator of TLR4 and downstream inflammatory pathway followi...Continue Reading

References

Apr 1, 1987·Toxicology and Applied Pharmacology·J D JohnsonG E Isom
Feb 16, 2002·Methods : a Companion to Methods in Enzymology·K J Livak, T D Schmittgen
Dec 31, 2003·Cell·Benjamin P LewisChristopher B Burge
Sep 17, 2004·Nature·Victor Ambros
Jun 4, 2005·Clinical and Experimental Immunology·P A Hopkins, S Sriskandan
Dec 20, 2005·Lancet Neurology·Guohua XiJulian T Hoff
Feb 7, 2006·Neurobiology of Disease·Jian WangSylvain Doré
Oct 13, 2006·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Jian Wang, Sylvain Doré
May 18, 2007·Annual Review of Cell and Developmental Biology·Natascha Bushati, Stephen M Cohen
May 23, 2009·Nature Reviews. Immunology·Serge Rivest
Dec 17, 2009·Current Opinion in Neurology·Fred Rincon, Stephan A Mayer
Nov 3, 2010·Nucleic Acids Research·Ana Kozomara, Sam Griffiths-Jones
May 25, 2011·Journal of Biomedical Informatics·Harsh DweepNorbert Gretz
Oct 27, 2011·Annals of Neurology·Lauren H SansingKatalin Kariko
Apr 14, 2012·Journal of Neuroimmunology·Manuel Rodríguez-YáñezTomás Sobrino
Feb 19, 2013·Journal of Neuroinflammation·Huang FangQing-Wu Yang
Jul 11, 2013·Stroke; a Journal of Cerebral Circulation·Yan-Chun WangQing-Wu Yang
Aug 17, 2014·Translational Stroke Research·Sofie Sølvsten SørensenThomas Christensen
Oct 25, 2014·Scientific Reports·Xin-Tong GeJian-Ning Zhang
Dec 6, 2014·Frontiers in Cellular Neuroscience·Eva Mracsko, Roland Veltkamp
Dec 24, 2014·Translational Stroke Research·Sheng ChenJohn H Zhang
May 6, 2015·Translational Stroke Research·Xiao-Yi Xiong, Qing-Wu Yang
Jun 14, 2016·Mediators of Inflammation·Monica MolteniCarlo Rossetti
Oct 11, 2017·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Hui LiFei Wang

❮ Previous
Next ❯

Citations

Jun 23, 2020·Metallomics : Integrated Biometal Science·Jiawen CuiShiwen Xu
Aug 8, 2021·International Journal of Molecular Sciences·Hisham KashifSangeetha Sukumari-Ramesh
Jul 24, 2021·Molecular Medicine Reports·Qiwen YuShuijun Zhang

❮ Previous
Next ❯

Methods Mentioned

BETA
electrophoresis
transfection
ELISA
nuclear translocation

Software Mentioned

SPSS
ImageJ
miRWalk
TargetScan
miRbase

Related Concepts

Related Feeds

Basal Ganglia

Basal Ganglia are a group of subcortical nuclei in the brain associated with control of voluntary motor movements, procedural and habit learning, emotion, and cognition. Here is the latest research.

Brain Injury & Trauma

brain injury after impact to the head is due to both immediate mechanical effects and delayed responses of neural tissues.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis