Publications

Latest publication 10/29/2019

The HDAC3 inhibitor RGFP966 ameliorated ischemic brain damage by downregulating

Histone deacetylases 3 (HDAC3) modulates the acetylation state of histone and non-histone proteins and could be a powerful regulator of...

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    [title] => The HDAC3 inhibitor RGFP966 ameliorated ischemic brain damage by downregulating 
    [paragraph] => The HDAC3 inhibitor RGFP966 ameliorated ischemic brain damage by downregulating the AIM2 inflammasome
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Authors
MJ Zhang, QC Zhao, MX Xia, J Chen, YT Chen, X Cao

 Lab
Department of Neurology, the Affiliated Drum Tower Hospital, Nanjing University Medical School, Nanjing City, Jiangsu Province, P. R. China.
Journal
The FASEB Journal
Abstract
Histone deacetylases 3 (HDAC3) modulates the acetylation state of histone and non-histone  proteins  and  could  be  a  powerful  regulator  of  the  inflammatory  process  in  stroke. Inflammasome activation is a ubiquitous but poorly understood consequence of acute ischemic stroke. Here, we investigated the potential contributions of HDAC3 to inflammasome activation in primary cultured microglia and experimental stroke models. In this study, we documented that HDAC3 expression was increased in mi-croglia of mouse experimental stroke model. Intraperitoneal injection of RGFP966 (a  selective  inhibitor  of  HDAC3)  decreased  infarct  size  and  alleviated  neurologi-cal  deficits  after  the  onset  of  middle  cerebral  artery  occlusion  (MCAO).  In  vitro  data  indicated  that  LPS  stimulation  evoked  a  time-dependent  increase  of  HDAC3  and  absent  in  melanoma  2  (AIM2)  inflammasome  in  primary  cultured  microglia.  Interestingly,  AIM2  was  subjected  to  spatiotemporal  regulation  by  RGFP966.  The  ability  of  RGFP966  to  inhibit  the  AIM2  inflammasome  was  confirmed  in  an  ex-perimental  mouse  model  of  stroke.  As  expected,  AIM2  knockout  mice  also  demonstrated  significant  resistance  to  ischemia  injury  compared  with  their  wild-type  littermates.  RGFP966  failed  to  exhibit  extra  protective  effects  in  AIM2_/_  stroke  mice. Furthermore, we found that RGFP966 enhanced STAT1 acetylation and subsequently attenuated STAT1 phosphorylation, which may at least partially contributed to the negative regulation of AIM2 by RGFP966. Together, we initially found that RGFP966 alleviated the inflammatory response and protected against ischemic stroke by regulating the AIM2 inflammasome.
BIOSEB Instruments Used
Grip strength test (BIO-GS3)
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An easy way to objectively quantify the muscular strength of mice and rats, and to assess the effect of drugs, toxins, muscular (i.e. myopathy) and neurodegenerative diseases on muscular degeneration. It is widely used in conjunction with the ROTAROD motor coordination test: a normally coordinated rodent will show a decreased latency to fall off the rotating rod if its muscular strength is low. The Grip Strength Test is a must for your research on activity, motor control & coordination, and is particularly well suited for studies on Parkinson's & Huntington's disease.
New features GS4 - 2023: Color display with permanent backlight screen for easier reading, reset by footswitch, Improved battery time, Larger data memory of 500 values, Animal counter, USB port (charging/data transfer)

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