lnc-MRGPRF-6:1 Promotes M1 Polarization of Macrophage and Inflammatory Response through the TLR4-MyD88-MAPK Pathway.
Mediators Inflamm
; 2022: 6979117, 2022.
Article
in En
| MEDLINE
| ID: mdl-35125964
ABSTRACT
BACKGROUND:
Macrophage-mediated inflammation plays an essential role in the development of atherosclerosis (AS). Long noncoding RNAs (lncRNAs), as crucial regulators, participate in this process. We identified that lnc-MRGPRF-61 was significantly upregulated in the plasma exosomes of coronary atherosclerotic disease (CAD) patients in a preliminary work. In the present study, we aim to assess the role of lnc-MRGPRF-61 in macrophage-mediated inflammatory process of AS.METHODS:
The correlation between lnc-MRGPRF-61 and inflammatory factors was estimated firstly in plasma exosomes of CAD patients. Subsequently, we established lnc-MRGPRF-61 knockout macrophage model via the CRISPR/Cas9 system. We then investigated the regulatory effects of lnc-MRGPRF-61 on macrophage polarization and foam cell formation. Eventually, transcriptome analysis by RNA sequencing was carried out to explore the contribution of differential genes and signaling pathways in this process.RESULTS:
lnc-MRGPRF-61 was highly expressed in the plasma exosomes of CAD patients and was positively correlated with the expression of inflammatory cytokines in plasma. lnc-MRGPRF-61 inhibition significantly reduced the formation of foam cells. The expression of lnc-MRGPRF-61 was upregulated in M1 macrophage, and lnc-MRGPRF-61 knockout decreased the polarization of M1 macrophage. lnc-MRGPRF-61 regulates macrophage polarization via the TLR4-MyD88-MAPK signaling pathway.CONCLUSIONS:
lnc-MRGPRF-61 knockdown can inhibit M1 polarization of macrophage and inflammatory response through the TLR4-MyD88-MAPK signaling pathway. lnc-MRGPRF-61 is a vital regulator in macrophage-mediated inflammatory process of AS.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Toll-Like Receptor 4
/
RNA, Long Noncoding
Type of study:
Prognostic_studies
Limits:
Humans
Language:
En
Journal:
Mediators Inflamm
Journal subject:
BIOQUIMICA
/
PATOLOGIA
Year:
2022
Document type:
Article
Affiliation country:
China
Publication country:
EEUU
/
ESTADOS UNIDOS
/
ESTADOS UNIDOS DA AMERICA
/
EUA
/
UNITED STATES
/
UNITED STATES OF AMERICA
/
US
/
USA