PMID- 26429502
OWN - NLM
STAT- MEDLINE
DCOM- 20160810
LR  - 20240204
IS  - 0219-1032 (Electronic)
IS  - 1016-8478 (Print)
IS  - 1016-8478 (Linking)
VI  - 38
IP  - 10
DP  - 2015 Oct
TI  - NMAAP1 Expressed in BCG-Activated Macrophage Promotes M1 Macrophage Polarization.
PG  - 886-94
LID - 10.14348/molcells.2015.0125 [doi]
AB  - Macrophages are divided into two subpopulations: classically activated 
      macrophages (M1) and alternatively activated macrophages (M2). BCG (Bacilli 
      Calmette-GuC)rin) activates disabled naC/ve macrophages to M1 macrophages, which 
      act as inflammatory, microbicidal and tumoricidal cells through cell-cell contact 
      and/or the release of soluble factors. Various transcription factors and 
      signaling pathways are involved in the regulation of macrophage activation and 
      polarization. We discovered that BCG-activated macrophages (BAM) expressed a new 
      molecule, and we named it Novel Macrophage Activated Associated Protein 1 
      (NMAAP1). The current study found that the overexpression of NMAAP1 in 
      macrophages results in M1 polarization with increased expression levels of M1 
      genes, such as inducible nitric oxide synthase (iNOS), tumor necrosis factor 
      alpha (TNF-N1), Interleukin 6 (IL-6), Interleukin 12 (IL-12), Monocyte 
      chemoattractant protein-1 (MCP-1) and Interleukin-1 beta (IL-1N2), and decreased 
      expression of some M2 genes, such as Kruppel-like factor 4 (KLF4) and suppressor 
      of cytokine signaling 1 (SOCS1), but not other M2 genes, including arginase-1 
      (Arg-1), Interleukin (IL-10), transforming growth factor beta (TGF-N2) and found 
      in inflammatory zone 1 (Fizz1). Moreover, NMAAP1 overexpression in the RAW264.7 
      cell line increased cytotoxicity against MCA207 tumor cells, which depends on 
      increased inflammatory cytokines rather than cell-cell contact. NMAAP1 also 
      substantially enhanced the phagocytic ability of macrophages, which implies that 
      NMAAP1 promoted macrophage adhesive and clearance activities. Our results 
      indicate that NMAAP1 is an essential molecule that modulates macrophages 
      phenotype and plays an important role in macrophage tumoricidal functions.
FAU - Liu, Qihui
AU  - Liu Q
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Tian, Yuan
AU  - Tian Y
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Zhao, Xiangfeng
AU  - Zhao X
AD  - Department of Immunology, Faculty of Basic Medical Sciences, Guilin Medical 
      University, Guilin 541004, China.
FAU - Jing, Haifeng
AU  - Jing H
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Xie, Qi
AU  - Xie Q
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Li, Peng
AU  - Li P
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Li, Dong
AU  - Li D
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Yan, Dongmei
AU  - Yan D
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
FAU - Zhu, Xun
AU  - Zhu X
AD  - Department of Immunology, College of Basic Medical Sciences, Jilin University, 
      Changchun 130021, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151002
PL  - United States
TA  - Mol Cells
JT  - Molecules and cells
JID - 9610936
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukins)
RN  - 0 (Klf4 protein, mouse)
RN  - 0 (Kruppel-Like Factor 4)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (Membrane Proteins)
RN  - 0 (NMAAP1 protein, mouse)
RN  - 0 (Socs1 protein, mouse)
RN  - 0 (Suppressor of Cytokine Signaling 1 Protein)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, mouse)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Chemokine CCL2/metabolism
MH  - *Cytotoxicity, Immunologic
MH  - Interleukins/metabolism
MH  - Kruppel-Like Factor 4
MH  - Kruppel-Like Transcription Factors/metabolism
MH  - *Macrophage Activation
MH  - Macrophages/*immunology
MH  - Membrane Proteins/genetics/*metabolism
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Mycobacterium bovis/*immunology
MH  - Neoplasms/*immunology
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - Phagocytosis
MH  - RAW 264.7 Cells
MH  - Suppressor of Cytokine Signaling 1 Protein
MH  - Suppressor of Cytokine Signaling Proteins/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC4625070
OTO - NOTNLM
OT  - M1
OT  - NMAAP1
OT  - differentiation
OT  - macrophage
OT  - tumor
EDAT- 2015/10/03 06:00
MHDA- 2016/08/11 06:00
PMCR- 2015/10/02
CRDT- 2015/10/03 06:00
PHST- 2015/05/11 00:00 [received]
PHST- 2015/07/09 00:00 [revised]
PHST- 2015/07/13 00:00 [accepted]
PHST- 2015/10/03 06:00 [entrez]
PHST- 2015/10/03 06:00 [pubmed]
PHST- 2016/08/11 06:00 [medline]
PHST- 2015/10/02 00:00 [pmc-release]
AID - S1016-8478(23)05504-8 [pii]
AID - molce-38-10-886 [pii]
AID - 10.14348/molcells.2015.0125 [doi]
PST - ppublish
SO  - Mol Cells. 2015 Oct;38(10):886-94. doi: 10.14348/molcells.2015.0125. Epub 2015 
      Oct 2.