PMID- 32843955
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220416
IS  - 2040-6223 (Print)
IS  - 2040-6231 (Electronic)
IS  - 2040-6223 (Linking)
VI  - 11
DP  - 2020
TI  - ABIN1 alleviates inflammatory responses and colitis via facilitating A20 
      activity.
PG  - 2040622320944782
LID - 10.1177/2040622320944782 [doi]
LID - 2040622320944782
AB  - BACKGROUND: Macrophages-mediated inflammation is involved in the progress of 
      colitis. The present study aims to explore the roles of A20-binding inhibitor of 
      NF-kappaB (ABIN1) in the macrophages and its underlying mechanisms. METHODS: ABIN1 
      myeloid cell-conditional transgenic mice were established and genotyped by PCR 
      and immunoblotting assays. Tumor necrosis factor (TNF)-alpha was applied to pre-treat 
      bone marrow-derived macrophages (BMDMs) in the presence of lipopolysaccharide. 
      The mRNA and protein levels of pro-inflammatory cytokines were determined by 
      qRT-PCR and ELISA, respectively. Dextran sulfate sodium (DSS)-induced colitis was 
      established to determine the effects of ABIN1 on the survival time, body weight, 
      colon length, and colon histopathological changes. Western blotting was applied 
      to determine the expressions of signaling proteins. RESULTS: ABIN1 overexpression 
      did not affect cell populations of macrophages and neutrophils in mice. Its 
      overexpression reduced the productions of pro-inflammatory cytokines in BMDMs and 
      ameliorated survival rate and colitis symptoms in the DSS-induced mouse model. 
      The underlying mechanisms revealed that ABIN1 impaired macrophages-mediated 
      inflammatory responses, in part by regulating the NF-kappaB signal pathway, and its 
      ameliorated effects on the symptoms of DSS-induced colitis were associated with 
      A20/tumor necrosis factor alpha-induced protein 3 (TNFAIP3). CONCLUSION: ABIN1 
      attenuated inflammatory responses and colitis by regulating A20/TNFAIP3 
      activities.
CI  - (c) The Author(s), 2020.
FAU - Pu, Tian
AU  - Pu T
AD  - Department of Gastroenterology, the First Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China.
FAU - Liu, Wenzheng
AU  - Liu W
AD  - Department of Gastroenterology, Peking University Third Hospital, Beijing, China.
FAU - Wu, Yijun
AU  - Wu Y
AD  - Department of Gastroenterology, the First Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China.
FAU - Zhao, Ye
AU  - Zhao Y
AUID- ORCID: 0000-0002-4923-5607
AD  - Department of Gastroenterology, the First Affiliated Hospital of Zhengzhou 
      University, No. 1 Jianshe East Road, Zhengzhou, Henan 450052, China.
LA  - eng
PT  - Journal Article
DEP - 20200730
PL  - United States
TA  - Ther Adv Chronic Dis
JT  - Therapeutic advances in chronic disease
JID - 101532140
PMC - PMC7418473
OTO - NOTNLM
OT  - A20/TNFAIP3
OT  - ABIN1
OT  - NF-kappaB signal pathway
OT  - colitis
OT  - inflammation
COIS- Conflict of interest statement: The authors declare that there is no conflict of 
      interest.
EDAT- 2020/08/28 06:00
MHDA- 2020/08/28 06:01
PMCR- 2020/07/30
CRDT- 2020/08/27 06:00
PHST- 2020/04/14 00:00 [received]
PHST- 2020/06/25 00:00 [accepted]
PHST- 2020/08/27 06:00 [entrez]
PHST- 2020/08/28 06:00 [pubmed]
PHST- 2020/08/28 06:01 [medline]
PHST- 2020/07/30 00:00 [pmc-release]
AID - 10.1177_2040622320944782 [pii]
AID - 10.1177/2040622320944782 [doi]
PST - epublish
SO  - Ther Adv Chronic Dis. 2020 Jul 30;11:2040622320944782. doi: 
      10.1177/2040622320944782. eCollection 2020.