Increased acetylation of H3K14 in the genomic regions that encode trained immunity enzymes in lysophosphatidylcholine-activated human aortic endothelial cells - Novel qualification markers for chronic disease risk factors and conditional DAMPs.
Acetylation
Adaptive Immunity
Aorta
/ metabolism
Atherosclerosis
/ etiology
Biomarkers
Chronic Disease
Disease Susceptibility
Endothelial Cells
/ metabolism
Gene Expression Regulation
Genes, Essential
Histones
/ metabolism
Humans
Lysophosphatidylcholines
/ metabolism
Metabolic Networks and Pathways
Models, Biological
Risk Factors
Signal Transduction
Chromatin long range interaction
Human aortic endothelial cell activation
Proatherogenic lipids lysophosphatidycholine (LPC)
RNA-Seq
Trained immunity
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
13
04
2019
revised:
06
05
2019
accepted:
14
05
2019
pubmed:
4
6
2019
medline:
4
3
2020
entrez:
2
6
2019
Statut:
ppublish
Résumé
To test our hypothesis that proatherogenic lysophosphatidylcholine (LPC) upregulates trained immunity pathways (TIPs) in human aortic endothelial cells (HAECs), we conducted an intensive analyses on our RNA-Seq data and histone 3 lysine 14 acetylation (H3K14ac)-CHIP-Seq data, both performed on HAEC treated with LPC. Our analysis revealed that: 1) LPC induces upregulation of three TIPs including glycolysis enzymes (GE), mevalonate enzymes (ME), and acetyl-CoA generating enzymes (ACE); 2) LPC induces upregulation of 29% of 31 histone acetyltransferases, three of which acetylate H3K14; 3) LPC induces H3K14 acetylation (H3K14ac) in the genomic DNA that encodes LPC-induced TIP genes (79%) in comparison to that of in LPC-induced effector genes (43%) including ICAM-1; 4) TIP pathways are significantly different from that of EC activation effectors including adhesion molecule ICAM-1; 5) reactive oxygen species generating enzyme NOX2 deficiency decreases, but antioxidant transcription factor Nrf2 deficiency increases, the expressions of a few TIP genes and EC activation effector genes; and 6) LPC induced TIP genes(81%) favor inter-chromosomal long-range interactions (CLRI, trans-chromatin interaction) while LPC induced effector genes (65%) favor intra-chromosomal CLRIs (cis-chromatin interaction). Our findings demonstrated that proatherogenic lipids upregulate TIPs in HAECs, which are a new category of qualification markers for chronic disease risk factors and conditional DAMPs and potential mechanisms for acute inflammation transition to chronic ones. These novel insights may lead to identifications of new cardiovascular risk factors in upregulating TIPs in cardiovascular cells and novel therapeutic targets for the treatment of metabolic cardiovascular diseases, inflammation, and cancers. (total words: 245).
Identifiants
pubmed: 31153039
pii: S2213-2317(19)30386-6
doi: 10.1016/j.redox.2019.101221
pmc: PMC6543097
pii:
doi:
Substances chimiques
Biomarkers
0
Histones
0
Lysophosphatidylcholines
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
101221Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL138749
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL117654
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL130233
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL131460
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK104116
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL132399
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL147565
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK113775
Pays : United States
Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.
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