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Article: Phagocytosis of apoptotic cells modulates mesenchymal stem cells osteogenic differentiation to enhance IL-17 and RANKL expression on CD4+ T cells

TitlePhagocytosis of apoptotic cells modulates mesenchymal stem cells osteogenic differentiation to enhance IL-17 and RANKL expression on CD4+ T cells
Authors
KeywordsApoptotic cells
Mesenchymal stem cells
Osteogenic differentiation
Rheumatoid arthritis
T helper 17 cells
Issue Date2010
PublisherAlphaMed Press, Inc. The Journal's web site is located at http://www.stemcells.com
Citation
Stem Cells, 2010, v. 28 n. 5, p. 939-954 How to Cite?
AbstractOsteogenic differentiation of mesenchymal stem cells (MSC) is important to homeostatic bone remodeling. Infiltration of mesenchymal progenitor cells to inflamed joints has been reported in collagen-induced arthritis murine model and in patients with rheumatoid arthritis (RA). Therapeutic application of MSC in RA has been suggested and under investigation. However, the underlying mechanisms on what triggers the migration of MSC from bone marrow (BM) to inflamed joints and how MSC acts in the joints remains elusive. As hemopoietic stem cells and MSC act reciprocally and excessive apoptotic cells (AC) are observed in the BM of patients with RA, we hypothesize that AC may alter MSC osteogenic differentiation resulting in bone erosion in RA. In this study, we demonstrated for the first time that MSC were able to phagocytose AC and this phagocytosis enhanced MSC osteogenic differentiation. AC-treated MSC under osteogenic differentiation expressed CXC-chemokine receptor (CXCR)-4 and CXCR5, which might enable them to migrate toward the inflamed joints. In addition, AC-treated MSC secreted interleukin (IL)-8, monocyte chemoattractant protein-1, and RANTES, which might induce chemotaxis of CD4+ T cells to the inflamed joints. Interestingly, by coculturing AC-treated MSC under osteogenic differentiation with CD4+ T cells, T helper (Th) 17 cells development was significantly enhanced and these Th17 cells promoted osteoclasts formation and bone resorption. Furthermore, the induction of Th17 cells was dependent on increased IL-6 production from major histocompatibility complex class II-expressing AC-treated MSC under osteogenic differentiation. This data provide a novel insight on the role of AC in modulating MSC osteogenic differentiation and function in inflammatory bone diseases. © AlphaMed Press.
Persistent Identifierhttp://hdl.handle.net/10722/125212
ISSN
2015 Impact Factor: 5.902
2015 SCImago Journal Rankings: 3.438
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTso, GHWen_HK
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorTu, Wen_HK
dc.contributor.authorChan, GCFen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-10-31T11:17:51Z-
dc.date.available2010-10-31T11:17:51Z-
dc.date.issued2010en_HK
dc.identifier.citationStem Cells, 2010, v. 28 n. 5, p. 939-954en_HK
dc.identifier.issn1066-5099en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125212-
dc.description.abstractOsteogenic differentiation of mesenchymal stem cells (MSC) is important to homeostatic bone remodeling. Infiltration of mesenchymal progenitor cells to inflamed joints has been reported in collagen-induced arthritis murine model and in patients with rheumatoid arthritis (RA). Therapeutic application of MSC in RA has been suggested and under investigation. However, the underlying mechanisms on what triggers the migration of MSC from bone marrow (BM) to inflamed joints and how MSC acts in the joints remains elusive. As hemopoietic stem cells and MSC act reciprocally and excessive apoptotic cells (AC) are observed in the BM of patients with RA, we hypothesize that AC may alter MSC osteogenic differentiation resulting in bone erosion in RA. In this study, we demonstrated for the first time that MSC were able to phagocytose AC and this phagocytosis enhanced MSC osteogenic differentiation. AC-treated MSC under osteogenic differentiation expressed CXC-chemokine receptor (CXCR)-4 and CXCR5, which might enable them to migrate toward the inflamed joints. In addition, AC-treated MSC secreted interleukin (IL)-8, monocyte chemoattractant protein-1, and RANTES, which might induce chemotaxis of CD4+ T cells to the inflamed joints. Interestingly, by coculturing AC-treated MSC under osteogenic differentiation with CD4+ T cells, T helper (Th) 17 cells development was significantly enhanced and these Th17 cells promoted osteoclasts formation and bone resorption. Furthermore, the induction of Th17 cells was dependent on increased IL-6 production from major histocompatibility complex class II-expressing AC-treated MSC under osteogenic differentiation. This data provide a novel insight on the role of AC in modulating MSC osteogenic differentiation and function in inflammatory bone diseases. © AlphaMed Press.en_HK
dc.languageengen_HK
dc.publisherAlphaMed Press, Inc. The Journal's web site is located at http://www.stemcells.comen_HK
dc.relation.ispartofStem Cellsen_HK
dc.subjectApoptotic cells-
dc.subjectMesenchymal stem cells-
dc.subjectOsteogenic differentiation-
dc.subjectRheumatoid arthritis-
dc.subjectT helper 17 cells-
dc.subject.meshApoptosis - immunologyen_HK
dc.subject.meshArthritis, Rheumatoid - immunology - metabolismen_HK
dc.subject.meshCD4-Positive T-Lymphocytes - immunology - metabolismen_HK
dc.subject.meshCell Differentiation - immunologyen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCoculture Techniquesen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInterleukin-17 - biosynthesis - geneticsen_HK
dc.subject.meshJurkat Cellsen_HK
dc.subject.meshMesenchymal Stem Cells - cytology - immunologyen_HK
dc.subject.meshOsteogenesis - immunologyen_HK
dc.subject.meshPhagocytosis - immunologyen_HK
dc.subject.meshRANK Ligand - biosynthesisen_HK
dc.titlePhagocytosis of apoptotic cells modulates mesenchymal stem cells osteogenic differentiation to enhance IL-17 and RANKL expression on CD4+ T cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1066-5099&volume=28&issue=5&spage=939&epage=54&date=2010&atitle=Phagocytosis+of+apoptotic+cells+modulates+mesenchymal+stem+cells+osteogenic+differentiation+to+enhance+IL-17+and+RANKL+expression+on+CD4++T+cellsen_HK
dc.identifier.emailTu, W:wwtu@hkucc.hku.hken_HK
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hken_HK
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.identifier.authorityChan, GCF=rp00431en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/stem.406en_HK
dc.identifier.pmid20222014-
dc.identifier.scopuseid_2-s2.0-77952398298en_HK
dc.identifier.hkuros179392en_HK
dc.identifier.hkuros179357-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952398298&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume28en_HK
dc.identifier.issue5en_HK
dc.identifier.spage939en_HK
dc.identifier.epage954en_HK
dc.identifier.eissn1549-4918-
dc.identifier.isiWOS:000278497400011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTso, GHW=8617703000en_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridTu, W=7006479236en_HK
dc.identifier.scopusauthoridChan, GCF=16160154400en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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