PMID- 29077222
OWN - NLM
STAT- MEDLINE
DCOM- 20181025
LR  - 20181025
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 119
IP  - 4
DP  - 2018 Apr
TI  - Class IIa HDACs inhibitor TMP269 promotes M1 polarization of macrophages after 
      spinal cord injury.
PG  - 3081-3090
LID - 10.1002/jcb.26446 [doi]
AB  - Spinal cord injury (SCI) is a devastating disease insulting neurological system, 
      and it could be further exacerbated by overwhelming inflammatory responses, where 
      macrophages play a central role. Depending on their heterogeneous phenotypes, 
      macrophages contribute intricately to SCI's pathological processes and functional 
      recovery. Although stimuli like interferons and cytokines are known to regulate 
      their phonotypical transition, it remains elusive which epigenetic programs 
      macrophages engage to complete phenotype shift. We report here that, the 
      treatment of TMP269, a highly selective class IIa HDACs inhibitor, augments the 
      production of pro-inflammatory cytokines in macrophages after SCI, meanwhile, 
      TMP269 also promotes their M1 phenotype activation, which is independent of Th1 
      or Th2 cytokines. Moreover, TMP269 exacerbates tissue damage and impairs 
      functional recovery after SCI. At last, the adoptive transfer of bone 
      marrow-derived macrophages (BMDMs) overexpressing class IIa HDACs shows 
      beneficial effects in inflammation resolution and functional recovery after SCI. 
      Thus, activating the class IIa HDACs to harness the anti-inflammatory effects of 
      macrophages may represent a potential target to treat SCI.
CI  - (c) 2017 Wiley Periodicals, Inc.
FAU - Qi, Xiangbei
AU  - Qi X
AUID- ORCID: 0000-0003-2259-1772
AD  - Department of Orthopaedics, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, China.
FAU - Wang, Pengcheng
AU  - Wang P
AUID- ORCID: 0000-0002-2482-4747
AD  - Trauma Emergency Center, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171226
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Cytokines)
RN  - 0 (Histone Deacetylase Inhibitors)
SB  - IM
MH  - Animals
MH  - CD4-Positive T-Lymphocytes/cytology/drug effects/immunology
MH  - Cell Polarity/drug effects
MH  - Cells, Cultured
MH  - Cytokines/*metabolism
MH  - Disease Models, Animal
MH  - Gene Expression Regulation
MH  - Histone Deacetylase Inhibitors/*administration & dosage/adverse 
      effects/chemistry/pharmacology
MH  - Macrophages/*cytology/drug effects/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Recovery of Function/drug effects
MH  - Spinal Cord Injuries/immunology/*physiopathology
MH  - *Up-Regulation
OTO - NOTNLM
OT  - M1 polarization
OT  - TMP269
OT  - class IIa HDACs
OT  - macrophage
OT  - spinal cord injury
EDAT- 2017/10/28 06:00
MHDA- 2018/10/26 06:00
CRDT- 2017/10/28 06:00
PHST- 2017/08/06 00:00 [received]
PHST- 2017/10/17 00:00 [accepted]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2018/10/26 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - 10.1002/jcb.26446 [doi]
PST - ppublish
SO  - J Cell Biochem. 2018 Apr;119(4):3081-3090. doi: 10.1002/jcb.26446. Epub 2017 Dec 
      26.