Human Gingiva‐Derived Mesenchymal Stem Cells Elicit Polarization of M2 Macrophages and Enhance Cutaneous Wound Healing

Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell‐like properties, immunosuppressive, and...

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Published in:	Stem cells (Dayton, Ohio) Vol. 28; no. 10; pp. 1856 - 1868
Main Authors:	Zhang, Qun‐Zhou, Su, Wen‐Ru, Shi, Shi‐Hong, Wilder‐Smith, Petra, Xiang, Andy Peng, Wong, Alex, Nguyen, Andrew L., Kwon, Chan Wook, Le, Anh D.
Format:	Journal Article
Language:	English
Published:	Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.10.2010
Subjects:	Animals Blotting, Western Cell Line Cells, Cultured Coculture Techniques Enzyme-Linked Immunosorbent Assay Flow Cytometry Gingiva - cytology Human gingival Humans M2 macrophages Macrophages - cytology Macrophages - immunology Male Mesenchymal stem cells Mesenchymal Stem Cells - cytology Mesenchymal Stem Cells - metabolism Mice Mice, Inbred C57BL Wound healing Wound Healing - immunology
ISSN:	1066-5099, 1549-4918, 1549-4918
Online Access:	Get full text
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Abstract	Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell‐like properties, immunosuppressive, and anti‐inflammatory functions as human bone marrow‐derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti‐inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)‐10 and IL‐6, a suppressed production of tumor necrosis factor (TNF)‐α, and decreased ability to induce Th‐17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL‐6 and TNF‐α, and an increased expression of IL‐10. The GMSC‐induced suppression of TNF‐α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing. STEM CELLS 2010;28:1856–1868
AbstractList	Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell-like properties, immunosuppressive, and anti-inflammatory functions as human bone marrow-derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti-inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)-10 and IL-6, a suppressed production of tumor necrosis factor (TNF)-α, and decreased ability to induce Th-17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL-6 and TNF-α, and an increased expression of IL-10. The GMSC-induced suppression of TNF-α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing. Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell-like properties, immunosuppressive, and anti-inflammatory functions as human bone marrow-derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti-inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)-10 and IL-6, a suppressed production of tumor necrosis factor (TNF)-α, and decreased ability to induce Th-17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL-6 and TNF-α, and an increased expression of IL-10. The GMSC-induced suppression of TNF-α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing.Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell-like properties, immunosuppressive, and anti-inflammatory functions as human bone marrow-derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti-inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)-10 and IL-6, a suppressed production of tumor necrosis factor (TNF)-α, and decreased ability to induce Th-17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL-6 and TNF-α, and an increased expression of IL-10. The GMSC-induced suppression of TNF-α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing. Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell‐like properties, immunosuppressive, and anti‐inflammatory functions as human bone marrow‐derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti‐inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)‐10 and IL‐6, a suppressed production of tumor necrosis factor (TNF)‐α, and decreased ability to induce Th‐17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL‐6 and TNF‐α, and an increased expression of IL‐10. The GMSC‐induced suppression of TNF‐α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing. STEM CELLS 2010;28:1856–1868
Author	Kwon, Chan Wook Zhang, Qun‐Zhou Su, Wen‐Ru Nguyen, Andrew L. Xiang, Andy Peng Le, Anh D. Shi, Shi‐Hong Wilder‐Smith, Petra Wong, Alex
AuthorAffiliation	b Beckman Laser Institute, University of California, Irvine, California, USA c Center for Stem Cell Biology and Tissue Engineering, Sun Yat-Sen University, Guangzhou, People’s Republic of China a Center for Craniofacial Molecular Biology, The Herman Ostrow School of Dentistry of University of Southern California, Los Angeles, California, USA d Division of Plastic and Reconstructive Surgery, University of Southern California Keck School of Medicine, Los Angeles, California, USA
AuthorAffiliation_xml	– name: a Center for Craniofacial Molecular Biology, The Herman Ostrow School of Dentistry of University of Southern California, Los Angeles, California, USA – name: d Division of Plastic and Reconstructive Surgery, University of Southern California Keck School of Medicine, Los Angeles, California, USA – name: c Center for Stem Cell Biology and Tissue Engineering, Sun Yat-Sen University, Guangzhou, People’s Republic of China – name: b Beckman Laser Institute, University of California, Irvine, California, USA
Author_xml	– sequence: 1 givenname: Qun‐Zhou surname: Zhang fullname: Zhang, Qun‐Zhou – sequence: 2 givenname: Wen‐Ru surname: Su fullname: Su, Wen‐Ru – sequence: 3 givenname: Shi‐Hong surname: Shi fullname: Shi, Shi‐Hong – sequence: 4 givenname: Petra surname: Wilder‐Smith fullname: Wilder‐Smith, Petra – sequence: 5 givenname: Andy Peng surname: Xiang fullname: Xiang, Andy Peng – sequence: 6 givenname: Alex surname: Wong fullname: Wong, Alex – sequence: 7 givenname: Andrew L. surname: Nguyen fullname: Nguyen, Andrew L. – sequence: 8 givenname: Chan Wook surname: Kwon fullname: Kwon, Chan Wook – sequence: 9 givenname: Anh D. surname: Le fullname: Le, Anh D. email: anhle@usc.edu
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/20734355$$D View this record in MEDLINE/PubMed
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Notes	First published online in STEM CELLS Author contributions: Q.‐Z.Z.: conception and design, collection and assembly of data, manuscript writing, final approval of the manuscript; W.‐R.S.: collection and assembly of data, final approval of the manuscript; S.‐H.S.: collection and assembly of data; P.W.S.: manuscript writing, final approval of the manuscript; A.P.X.: manuscript writing, final approval of the manuscript; A.W.: manuscript writing, final approval of the manuscript; A.L.N: collection and assembly of data; B.K.: collection and assembly of data; A.D.L.: conception and design, manuscript writing, final approval of the manuscript, financial support. Disclosure of potential conflicts of interest is found at the end of this article. Telephone: 323‐442‐2556; Fax: 323‐442‐2981 EXPRESS August 23, 2010. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
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Snippet	Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear....
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SubjectTerms	Animals Blotting, Western Cell Line Cells, Cultured Coculture Techniques Enzyme-Linked Immunosorbent Assay Flow Cytometry Gingiva - cytology Human gingival Humans M2 macrophages Macrophages - cytology Macrophages - immunology Male Mesenchymal stem cells Mesenchymal Stem Cells - cytology Mesenchymal Stem Cells - metabolism Mice Mice, Inbred C57BL Wound healing Wound Healing - immunology
Title	Human Gingiva‐Derived Mesenchymal Stem Cells Elicit Polarization of M2 Macrophages and Enhance Cutaneous Wound Healing
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