PMID- 27734926
OWN - NLM
STAT- MEDLINE
DCOM- 20180502
LR  - 20181113
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 6
DP  - 2016 Oct 13
TI  - Bone marrow-derived and peritoneal macrophages have different inflammatory 
      response to oxLDL and M1/M2 marker expression - implications for atherosclerosis 
      research.
PG  - 35234
LID - 10.1038/srep35234 [doi]
LID - 35234
AB  - Macrophages are heterogeneous and can polarize into specific subsets, e.g. 
      pro-inflammatory M1-like and re-modelling M2-like macrophages. To determine if 
      peritoneal macrophages (PEMs) or bone marrow derived macrophages (BMDMs) 
      resembled aortic macrophages from ApoE-/- mice, their M1/M2 phenotype, 
      inflammatory status, and lipid metabolism signatures were compared. oxLDL 
      accumulation was similar in PEMs and BMDMs. On protein expression level, BMDMs 
      showed an M2-like CD206(high)CD11c(low) profile, while cholesterol loading led to 
      enhanced CD11c expression and reduced MCP-1 secretion. In contrast, PEMs 
      expressed low levels of CD206 and CD11c, and responded to cholesterol loading by 
      increasing CD11c expression and MCP-1 secretion. mRNA expression of M1/M2 markers 
      was higher in PEMS than BMDMs, while lipid metabolism genes were similarly 
      expressed. Whole aorta flow cytometry showed an accumulation of M2-like 
      CD206(high)CD11c(low) macrophages in advanced versus early atherosclerotic 
      disease in ApoE-/- mice. In isolated lesions, mRNA levels of the M2 markers 
      Socs2, CD206, Retnla, and IL4 were downregulated with increasing disease 
      severity. Likewise, mRNA expression of lipid metabolism genes (SREBP2, ACSL1, 
      SRB1, DGAT1, and cpt1a) was decreased in advanced versus early lesions. In 
      conclusion, PEMs and BMDMs are phenotypically distinct and differ from 
      macrophages in lesions with respect to expression of M1/M2 markers and lipid 
      metabolism genes.
FAU - Bisgaard, Line S
AU  - Bisgaard LS
AD  - Dept. of Biomedical Sciences, University of Copenhagen, Denmark.
AD  - Dept. of Diabetic Complication Biology, Novo Nordisk, Denmark.
FAU - Mogensen, Christina K
AU  - Mogensen CK
AD  - Dept. of Diabetic Complication Biology, Novo Nordisk, Denmark.
FAU - Rosendahl, Alexander
AU  - Rosendahl A
AD  - Dept. of Diabetic Complication Biology, Novo Nordisk, Denmark.
AD  - Dept. of Biopharmaceuticals New Heamophilia, Novo Nordisk, Denmark.
FAU - Cucak, Helena
AU  - Cucak H
AD  - Dept. of Diabetic Complication Biology, Novo Nordisk, Denmark.
FAU - Nielsen, Lars Bo
AU  - Nielsen LB
AD  - Dept. of Biomedical Sciences, University of Copenhagen, Denmark.
AD  - Dept. of Clinical Biochemistry, Copenhagen University Hospital Rigshospitalet, 
      Denmark.
FAU - Rasmussen, Salka E
AU  - Rasmussen SE
AD  - Dept. of ADME, Novo Nordisk, Denmark.
FAU - Pedersen, Tanja X
AU  - Pedersen TX
AD  - Dept. of Biomedical Sciences, University of Copenhagen, Denmark.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20161013
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (oxidized low density lipoprotein)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/*cytology
MH  - Female
MH  - Inflammation/*pathology
MH  - Lipoproteins, LDL/*metabolism
MH  - Macrophages, Peritoneal/*cytology
MH  - Mice
MH  - Mice, Inbred C57BL
PMC - PMC5062347
COIS- L.S.B., S.E.R., C.K.M., A.R. and H.C. has been or are employed at Novo Nordisk.
EDAT- 2016/10/14 06:00
MHDA- 2018/05/03 06:00
PMCR- 2016/10/13
CRDT- 2016/10/14 06:00
PHST- 2016/03/22 00:00 [received]
PHST- 2016/09/07 00:00 [accepted]
PHST- 2016/10/14 06:00 [entrez]
PHST- 2016/10/14 06:00 [pubmed]
PHST- 2018/05/03 06:00 [medline]
PHST- 2016/10/13 00:00 [pmc-release]
AID - srep35234 [pii]
AID - 10.1038/srep35234 [doi]
PST - epublish
SO  - Sci Rep. 2016 Oct 13;6:35234. doi: 10.1038/srep35234.