PMID- 35740904
OWN - NLM
STAT- MEDLINE
DCOM- 20220627
LR  - 20220716
IS  - 2218-273X (Electronic)
IS  - 2218-273X (Linking)
VI  - 12
IP  - 6
DP  - 2022 Jun 2
TI  - Transcriptomic Profiling Reveals That HMGB1 Induces Macrophage Polarization 
      Different from Classical M1.
LID - 10.3390/biom12060779 [doi]
LID - 779
AB  - Macrophages are key inflammatory immune cells that display dynamic phenotypes and 
      functions in response to their local microenvironment. In different conditions, 
      macrophage polarization can be induced by high-mobility group box 1 (HMGB1), a 
      nuclear DNA-binding protein that activates innate immunity via the Toll-like 
      receptor (TLR) 4, the receptor for advanced glycation end products (RAGE), and 
      C-X-C chemokine receptor (CXCR) 4. This study investigated the phenotypes of 
      murine bone-marrow-derived macrophages (BMDMs) stimulated with different HMGB1 
      redox isoforms using bulk RNA sequencing (RNA-Seq). Disulfide HMGB1 
      (dsHMGB1)-stimulated BMDMs showed a similar but distinct transcriptomic profile 
      to LPS/IFNgamma- and LPS-stimulated BMDMs. Fully reduced HMGB1 (frHMGB1) did not 
      induce any significant transcriptomic change. Interestingly, compared to 
      LPS/IFNgamma- and LPS-, dsHMGB1-stimulated BMDMs showed lipid metabolism and foam 
      cell differentiation gene set enrichment, and oil red O staining revealed that 
      both dsHMGB1 and frHMGB1 alleviated oxidized low-density lipoprotein 
      (oxLDL)-induced foam cells formation. Overall, this work, for the first time, 
      used transcriptomic analysis by RNA-Seq to investigate the impact of HMGB1 
      stimulation on BMDM polarization. Our results demonstrated that dsHMGB1 and 
      frHMGB1 induced distinct BMDM polarization phenotypes compared to LPS/IFNgamma- and 
      LPS- induced phenotypes.
FAU - Qu, Heshuang
AU  - Qu H
AUID- ORCID: 0000-0001-6011-5588
AD  - Department of Medicine, Solna, Karolinska Institutet, and Centre for Molecular 
      Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
FAU - Heinback, Rebecka
AU  - Heinback R
AUID- ORCID: 0000-0001-7004-252X
AD  - Department of Medicine, Solna, Karolinska Institutet, and Centre for Molecular 
      Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
FAU - Salo, Henna
AU  - Salo H
AD  - Department of Medicine, Solna, Karolinska Institutet, and Centre for Molecular 
      Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
FAU - Ewing, Ewoud
AU  - Ewing E
AD  - Department of Clinical Neuroscience, Karolinska Institutet, and Centre for 
      Molecular Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
FAU - Espinosa, Alexander
AU  - Espinosa A
AD  - Department of Medicine, Solna, Karolinska Institutet, and Centre for Molecular 
      Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
FAU - Aulin, Cecilia
AU  - Aulin C
AD  - Department of Medicine, Solna, Karolinska Institutet, and Centre for Molecular 
      Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
FAU - Erlandsson Harris, Helena
AU  - Erlandsson Harris H
AD  - Department of Medicine, Solna, Karolinska Institutet, and Centre for Molecular 
      Medicine, Karolinska University Hospital, 171 64 Stockholm, Sweden.
AD  - Broegelmann Research Laboratory, Department of Clinical Science, University of 
      Bergen, 5021 Bergen, Norway.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220602
PL  - Switzerland
TA  - Biomolecules
JT  - Biomolecules
JID - 101596414
RN  - 0 (HMGB1 Protein)
RN  - 0 (HMGB1 protein, mouse)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Animals
MH  - *HMGB1 Protein/genetics/metabolism
MH  - Lipopolysaccharides/metabolism/pharmacology
MH  - *Macrophage Activation
MH  - Macrophages/metabolism
MH  - Mice
MH  - *Transcriptome
PMC - PMC9221381
OTO - NOTNLM
OT  - HMGB1
OT  - RNA sequencing
OT  - foam cell formation
OT  - gene ontology
OT  - macrophage polarization
COIS- The authors declare no conflict of interest.
EDAT- 2022/06/25 06:00
MHDA- 2022/06/28 06:00
PMCR- 2022/06/02
CRDT- 2022/06/24 01:09
PHST- 2022/05/15 00:00 [received]
PHST- 2022/05/27 00:00 [revised]
PHST- 2022/05/31 00:00 [accepted]
PHST- 2022/06/24 01:09 [entrez]
PHST- 2022/06/25 06:00 [pubmed]
PHST- 2022/06/28 06:00 [medline]
PHST- 2022/06/02 00:00 [pmc-release]
AID - biom12060779 [pii]
AID - biomolecules-12-00779 [pii]
AID - 10.3390/biom12060779 [doi]
PST - epublish
SO  - Biomolecules. 2022 Jun 2;12(6):779. doi: 10.3390/biom12060779.