PMID- 27866511
OWN - NLM
STAT- MEDLINE
DCOM- 20170310
LR  - 20190609
IS  - 1976-670X (Electronic)
IS  - 1976-6696 (Print)
IS  - 1976-6696 (Linking)
VI  - 50
IP  - 1
DP  - 2017 Jan
TI  - Impaired phagocytosis of apoptotic cells causes accumulation of bone 
      marrow-derived macrophages in aged mice.
PG  - 43-48
AB  - Accumulation of tissue macrophages is a significant characteristic of 
      disease-associated chronic inflammation, and facilitates the progression of 
      disease pathology. However, the functional roles of these bone marrow-derived 
      macrophages (BMDMs) in aging are unclear. Here, we identified agedependent 
      macrophage accumulation in the bone marrow, showing that aging significantly 
      increases the number of M1 macrophages and impairs polarization of BMDMs. We 
      found that age-related dysregulation of BMDMs is associated with abnormal 
      overexpression of the anti-inflammatory interleukin-10. BMDM dysregulation in 
      aging impairs the expression levels of pro-inflammatory cytokines and genes 
      involved in B-cell maturation and activation. Phagocytosis of apoptotic Jurkat 
      cells by BMDMs was reduced because of low expression of phagocytic receptor CD14, 
      indicating that increased apoptotic cells may result from defective phagocytosis 
      of apoptotic cells in the BM of aged mice. Therefore, CD14 may represent a 
      promising target for preventing BMDM dysregulation, and macrophage accumulation 
      may provide diagnostic and therapeutic clues. [BMB Reports 2017; 50(1): 43-48].
FAU - Kim, Ok-Hee
AU  - Kim OH
AD  - Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, 
      Incheon 21999, Korea.
FAU - Kim, Hyojung
AU  - Kim H
AD  - Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, 
      Incheon 21999, Korea.
FAU - Kang, Jinku
AU  - Kang J
AD  - Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, 
      Incheon 21999, Korea.
FAU - Yang, Dongki
AU  - Yang D
AD  - Department of Physiology, College of Medicine, Gachon University, Incheon 21999, 
      Korea.
FAU - Kang, Yu-Hoi
AU  - Kang YH
AD  - Samsung Advanced Institute of Technology, Samsung Electronics Co. Ltd., Suwon 
      16678, Korea.
FAU - Lee, Dae Ho
AU  - Lee DH
AD  - Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, 
      Incheon 21999, Korea.
FAU - Cheon, Gi Jeong
AU  - Cheon GJ
AD  - Department of Nuclear Medicine, Seoul National University College of Medicine, 
      Seoul 03080, Korea.
FAU - Park, Sang Chul
AU  - Park SC
AD  - Well Aging Research Center, DGIST, Daegu 42988, Korea.
FAU - Oh, Byung-Chul
AU  - Oh BC
AD  - Lee Gil Ya Cancer and Diabetes Institute, College of Medicine; Department of 
      Physiology, College of Medicine, Gachon University, Incheon 21999, Korea.
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - BMB Rep
JT  - BMB reports
JID - 101465334
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Aging/metabolism/*pathology
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Apoptosis/*physiology
MH  - Bone Marrow Cells/*cytology/metabolism
MH  - Cell Differentiation/physiology
MH  - Cytokines/metabolism
MH  - Humans
MH  - Inflammation/pathology
MH  - Interleukin-10/metabolism
MH  - Jurkat Cells
MH  - Lipopolysaccharide Receptors/metabolism
MH  - Macrophages/*cytology/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Phagocytosis/*physiology
PMC - PMC5319664
EDAT- 2016/11/22 06:00
MHDA- 2017/03/11 06:00
PMCR- 2017/02/01
CRDT- 2016/11/22 06:00
PHST- 2016/09/29 00:00 [received]
PHST- 2016/11/22 06:00 [pubmed]
PHST- 2017/03/11 06:00 [medline]
PHST- 2016/11/22 06:00 [entrez]
PHST- 2017/02/01 00:00 [pmc-release]
AID - 3674 [pii]
AID - bmb-50-043 [pii]
AID - 10.5483/bmbrep.2017.50.1.167 [doi]
PST - ppublish
SO  - BMB Rep. 2017 Jan;50(1):43-48. doi: 10.5483/bmbrep.2017.50.1.167.