PMID- 37882711
OWN - NLM
STAT- MEDLINE
DCOM- 20231030
LR  - 20231030
IS  - 1007-8738 (Print)
IS  - 1007-8738 (Linking)
VI  - 39
IP  - 10
DP  - 2023 Oct
TI  - [Effects and mechanism of knocking down lncRNA H19 to inhibit lipid accumulation 
      in human THP-1 cells-derived macrophages].
PG  - 884-890
AB  - Objective To investigate the effects of long noncoding RNA H19 on lipid 
      accumulation of macrophages under high fat stress and its mechanism. Methods 
      Human THP-1 cells-derived macrophages were incubated with ox-LDL, and the effects 
      of H19 siRNA intervention on lipid accumulation was observed. The THP-1 cells 
      were divided into control group (conventional culture), ox-LDL group, siRNA 
      negative control (NC siRNA) combined with ox-LDL treatment group, and H19 siRNA 
      combined with ox-LDL treatment group. Oil red O staining was used to determine 
      the lipid accumulation in cells, and cholesterol concentration was analyzed by 
      enzymatic method; ATP assay kit for detecting celluar ATP content; colorimetry 
      was used to detect the levels of oxidative stress indicators and ELISA was used 
      to detect the levels of monocyte chemoattractant protein-1 (MCP-1) in the cell 
      supernatant. Western blot analysis was used to detect the protein expression of 
      ATP binding cassette transporter A1 (ABCA1), peroxisome proliferator-activated 
      receptor alpha (PPARalpha), peroxisome proliferator-activated receptor gamma coactivator-1alpha 
      (PGC-1alpha) and nuclear factor kappaB p-p65 (NF-kappaB p-p65). Results Knockdown H19 
      significantly inhibited intracellular lipid accumulation, decreased total 
      cholesterol (TC) and cholesterol ester (CE) content, and decreased CE/TC ratio. 
      Knockdown H19 significantly alleviated cell damage including an increase in ATP 
      content, a decrease in oxidative stress levels and a decrease in MCP-1 levels, 
      which caused by high-fat stress. H19 siRNA upregulated expression of ABCA1, PPARalpha 
      and PGC-1alpha in THP-1 derived macrophages, downregulated NF-kappaB signal pathway. 
      Conclusion Knockdown H19 upregulates PGC-1alpha expression in THP-1 cells and 
      downregulates NF-kappaB pathway, which promotes cholesterol reverse transport, 
      reduces inflammatory reaction and inhibits lipid accumulation.
FAU - Wang, Xuemei
AU  - Wang X
AD  - Department of Public Health, Xi'an Medical College; Shaanxi Key Laboratory of 
      Ischemic Cardiovascular Diseases & Institute of Basic and Translational Medicine, 
      Xi'an Medical College, Xi'an 710021, China.
FAU - Che, Yue
AU  - Che Y
AD  - Department of Public Health, Xi'an Medical College, Xi'an 710021, China.
FAU - Wang, Jieying
AU  - Wang J
AD  - Department of Public Health, Xi'an Medical College; Shaanxi Key Laboratory of 
      Ischemic Cardiovascular Diseases & Institute of Basic and Translational Medicine, 
      Xi'an Medical College, Xi'an 710021, China.
FAU - Men, Ke
AU  - Men K
AD  - Department of Public Health, Xi'an Medical College, Xi'an 710021, China. 
      *Corresponding author, E-mail: menke@foxmail.com.
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
JT  - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular 
      immunology
JID - 101139110
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - 0 (NF-kappa B)
RN  - 0 (PPAR alpha)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (H19 long non-coding RNA)
SB  - IM
MH  - Humans
MH  - Adenosine Triphosphate
MH  - Cholesterol
MH  - *NF-kappa B
MH  - PPAR alpha
MH  - *RNA, Long Noncoding/genetics
MH  - RNA, Small Interfering/genetics
MH  - THP-1 Cells
MH  - *Macrophages/metabolism
MH  - *Lipid Metabolism
EDAT- 2023/10/26 12:42
MHDA- 2023/10/27 06:42
CRDT- 2023/10/26 10:13
PHST- 2023/10/27 06:42 [medline]
PHST- 2023/10/26 12:42 [pubmed]
PHST- 2023/10/26 10:13 [entrez]
PST - ppublish
SO  - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2023 Oct;39(10):884-890.