PMID- 30458295
OWN - NLM
STAT- MEDLINE
DCOM- 20190408
LR  - 20211204
IS  - 1878-5492 (Electronic)
IS  - 0966-3274 (Linking)
VI  - 52
DP  - 2019 Feb
TI  - Regulatory effects of dermal papillary pluripotent stem cells on polarization of 
      macrophages from M1 to M2 phenotype in vitro.
PG  - 57-67
LID - S0966-3274(18)30120-5 [pii]
LID - 10.1016/j.trim.2018.11.003 [doi]
AB  - The M1:M2 macrophage ratio is important for spinal cord injury (SCI) repair. Bone 
      marrow mesenchymal stem cells (BMSCs) can alter macrophage activation, promoting 
      M1 to M2 macrophage conversion and SCI repair; however, clinical BMSC 
      applications have limitations. Previously, we found DPCs to be superior to BMSCs 
      in promoting tissue repair after SCI, which we hypothesized to be mediated by M1 
      to M2 macrophage conversion. We investigated the regulatory effect of DPCs on 
      M1/M2 macrophage polarization. Dermal papilla cells (DPCs) were isolated from rat 
      vibrissae and characterized. Bone marrow-derived macrophages (BMDMs) were 
      isolated and identified based on specific marker expression, and stimulated to 
      differentiate into M1 macrophages with GM-CSF, IFN-gamma, and LPS. These cells were 
      co-cultured with DPCs to evaluate the effect on macrophage differentiation. DPCs 
      expressed dermal papillae-specific markers, including ALP and Sox2, had 
      MSC-expression patterns like those of BMSCs, and were capable of 
      multi-differentiation. BMDMs expressed ANAE and CD68. Three days after induction, 
      differentiated cells exhibited morphology typical of M1-like macrophages and 
      expressed the macrophage marker CD68 and the M1 macrophage markers iNOS, but 
      lacked expression of the M2 macrophage marker CD206. Co-culture with DPCs 
      resulted in a shift to anti-inflammatory M2-like macrophage differentiation, 
      characterized by morphological changes typical of M2 macrophages, downregulation 
      of the characteristic cytokine TNF-alpha and the proportion of iNOS(+) cells, and 
      upregulation of the characteristic cytokine IL-10 and the cell-surface marker 
      CD206. The number of CD206-expressing M2 macrophages also increased. These 
      findings demonstrate that DPCs reprogram macrophages to an anti-inflammatory M2 
      phenotype, which could improve adverse inflammatory microenvironments and promote 
      tissue repair. Thus, DPCs may be an interesting alternative cell source and merit 
      further investigation in applications for SCI therapy.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Li, Meiying
AU  - Li M
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China; Department of Surgery, The First Hospital of 
      Jilin University, Changchun, Jilin 130021, PR China. Electronic address: 
      limeiying@jlu.edu.cn.
FAU - Xu, Jiayi
AU  - Xu J
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China; Department of Pathology, Central Hospital of 
      Panzhihua, Panzhihua, Sichuan 617067, PR China.
FAU - Mei, Xianglin
AU  - Mei X
AD  - Department of Pathology, Second Hospital of Jilin University, Changchun, Jilin 
      130000, PR China; National Engineering Laboratory for Druggable Gene and Protein 
      Screening, Northeast Normal University, Changchun, Jilin 130024, PR China.
FAU - Chi, Guangfan
AU  - Chi G
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China.
FAU - Li, Lisha
AU  - Li L
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China.
FAU - Song, Yaolin
AU  - Song Y
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China.
FAU - He, Xia
AU  - He X
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China.
FAU - Li, Yulin
AU  - Li Y
AD  - The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 
      Changchun, Jilin 130021, PR China. Electronic address: ylli@jlu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181117
PL  - Netherlands
TA  - Transpl Immunol
JT  - Transplant immunology
JID - 9309923
RN  - 0 (Cytokines)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Mannose Receptor)
RN  - 0 (Mannose-Binding Lectins)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (SOXB1 Transcription Factors)
RN  - 0 (Sox2 protein, rat)
RN  - EC 1.13.11.- (Adi1 protein, rat)
RN  - EC 1.13.11.- (Dioxygenases)
RN  - EC 3.1.- (Naphthol AS D Esterase)
SB  - IM
MH  - Animals
MH  - Cell Differentiation
MH  - Cell- and Tissue-Based Therapy/*methods
MH  - Cells, Cultured
MH  - Coculture Techniques
MH  - Cytokines/metabolism
MH  - Dermis/*pathology
MH  - Dioxygenases/metabolism
MH  - Lectins, C-Type/metabolism
MH  - Macrophages/*physiology
MH  - Mannose Receptor
MH  - Mannose-Binding Lectins/metabolism
MH  - Naphthol AS D Esterase/metabolism
MH  - Pluripotent Stem Cells/*physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Cell Surface/metabolism
MH  - SOXB1 Transcription Factors/metabolism
MH  - Th1 Cells/immunology
MH  - Th2 Cells/immunology
OTO - NOTNLM
OT  - Dermal papilla cell
OT  - Macrophage
OT  - Mesenchymal stem cell
OT  - Polarization
OT  - Spinal cord injury
EDAT- 2018/11/21 06:00
MHDA- 2019/04/09 06:00
CRDT- 2018/11/21 06:00
PHST- 2018/08/27 00:00 [received]
PHST- 2018/11/14 00:00 [revised]
PHST- 2018/11/16 00:00 [accepted]
PHST- 2018/11/21 06:00 [pubmed]
PHST- 2019/04/09 06:00 [medline]
PHST- 2018/11/21 06:00 [entrez]
AID - S0966-3274(18)30120-5 [pii]
AID - 10.1016/j.trim.2018.11.003 [doi]
PST - ppublish
SO  - Transpl Immunol. 2019 Feb;52:57-67. doi: 10.1016/j.trim.2018.11.003. Epub 2018 
      Nov 17.