PMID- 30936963
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 17
IP  - 4
DP  - 2019 Apr
TI  - TIPE2 suppresses atherosclerosis by exerting a protective effect on macrophages 
      via the inhibition of the Akt signaling pathway.
PG  - 2937-2944
LID - 10.3892/etm.2019.7316 [doi]
AB  - Macrophage apoptosis and inflammation serve pivotal roles in the occurrence of 
      atherosclerosis. However, the detailed underlying mechanism of macrophage action 
      during atherosclerosis is poorly understood. Tumor necrosis factor-alpha-induced 
      protein 8-like 2 (TIPE2) is a well-known negative regulator of the immune 
      response. The current study assessed the association between TIPE2 and 
      apoptosis-associated molecules in macrophages during atherosclerosis, as well as 
      the role of TIPE2 in macrophage inflammation. RAW264.7 macrophages were 
      subsequently transfected with a TIPE2 expression plasmid. Following oxidized 
      low-density lipoprotein (oxLDL) induction (100 microg/m1) for 48 h, macrophage 
      apoptosis was assessed via Annexin V/propidium iodide dual staining. The 
      apoptosis-associated factors and Akt signaling pathway-associated factors were 
      also evaluated via western blot analysis. The expression of inflammatory factors 
      was determined via a reverse transcription-quantitative polymerase chain reaction 
      assay and western blotting. Furthermore, a transwell assay was performed to test 
      cell invasion ability. NF-kappaB phosphorylation and nuclear translocation were also 
      assessed via western blotting. The results demonstrated that TIPE2 overexpression 
      may promote oxLDL-induced RAW264.7 macrophage apoptosis by inhibiting the protein 
      kinase B (Akt) signaling pathway. Furthermore, it was demonstrated that TIPE2 
      significantly reduced oxLDL-induced tumor necrosis factor alpha (TNF-alpha), 
      interleukin-6 (IL-6) and monocyte chemoattractant protein 1 expression (MCP-1), 
      and increased IL-10 expression by suppressing NF-kappaB phosphorylation and nuclear 
      translocation in RAW264.7 macrophages. These results indicated that TIPE2 serves 
      a protective role in oxLDL-induced RAW264.7 macrophages, and its mechanism may 
      partly be exerted via the inhibition of the PI3K/Akt signaling pathway and the 
      reduction of the macrophage inflammatory response achieved via the suppression of 
      NF-kappaB signal activation.
FAU - Li, Dan
AU  - Li D
AD  - Department of Geriatrics, The Second Xiangya Hospital of Central South 
      University, Changsha, Hunan 410011, P.R. China.
FAU - Tan, Ying
AU  - Tan Y
AD  - Department of Cardiovascular Medicine, The First Affiliated Hospital of 
      University of South China, Hengyang, Hunan 421000, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20190226
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC6434246
OTO - NOTNLM
OT  - apoptosis
OT  - atherosclerosis
OT  - inflammation
OT  - macrophage
OT  - nuclear factor-kappaB
OT  - protein kinase B
OT  - tumor necrosis factor-alpha-induced protein 8-like 2
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:01
PMCR- 2019/02/26
CRDT- 2019/04/03 06:00
PHST- 2018/05/02 00:00 [received]
PHST- 2018/11/30 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:01 [medline]
PHST- 2019/02/26 00:00 [pmc-release]
AID - ETM-0-0-7316 [pii]
AID - 10.3892/etm.2019.7316 [doi]
PST - ppublish
SO  - Exp Ther Med. 2019 Apr;17(4):2937-2944. doi: 10.3892/etm.2019.7316. Epub 2019 Feb 
      26.