FGF2 induces RANKL gene expression as well as IL1β regulated MHC class II in human bone marrow-derived mesenchymal progenitor stromal cells.

Détails

ID Serval
serval:BIB_9E759CD4D7BC
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Compte-rendu: analyse d'une oeuvre publiée.
Collection
Publications
Titre
FGF2 induces RANKL gene expression as well as IL1β regulated MHC class II in human bone marrow-derived mesenchymal progenitor stromal cells.
Périodique
Annals of the rheumatic diseases
Auteur(s)
Bocelli-Tyndall C., Trella E., Frachet A., Zajac P., Pfaff D., Geurts J., Heiler S., Barbero A., Mumme M., Resink T.J., Schaeren S., Spagnoli G.C., Tyndall A.
ISSN
1468-2060 (Electronic)
ISSN-L
0003-4967
Statut éditorial
Publié
Date de publication
01/2015
Peer-reviewed
Oui
Volume
74
Numéro
1
Pages
260-266
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
Human bone marrow mesenchymal stromal cells (hBM-MSC) are being applied in tissue regeneration and treatment of autoimmune diseases (AD). Their cellular and immunophenotype depend on isolation and culture conditions which may influence their therapeutic application and reflect their in vivo biological functions. We have further characterised the phenotype induced by fibroblast growth factor 2 (FGF2) on healthy donor hBM-MSC focusing on the osteoimmunological markers osteoprotegerin (OPG), receptor activator of nuclear factor kB (RANK), RANK ligand (RANKL) and HLA-DR and their regulation of expression by the inflammatory cytokines IL1β and IFNγ.
RANK, RANKL, OPG and HLA-DR expression in hBM-MSC expanded under specific culture conditions, were measured by RT-PCR and flow cytometry. MAPKs induction by FGF2, IL1β and IFNγ in hBM-MSC was analysed by immunoblotting and RT-PCR.
In hBM-MSC, OPG expression is constitutive and FGF2 independent. RANKL expression depends on FGF2 and ERK1/2 activation. IL1β and IFNγ activate ERK1/2 but fail to induce RANKL. Only IL1β induces P38MAPK. The previously described HLA-DR induced by FGF2 through ERK1/2 on hBM-MSC, is suppressed by IL1β through inhibition of CIITA transcription. HLA-DR induced by IFNγ is not affected by IL1β in hBM-MSC, but is suppressed in articular chondrocytes and lung fibroblasts.
RANKL expression and IL1β regulated MHC-class II, both induced via activation of the ERK1/2 signalling pathway, are specific for progenitor hBM-MSC expanded in the presence of FGF2. HLA-DR regulated by IL1β and ERK1/2 is observed on hBM-MSC during early expansion without FGF2 suggesting previous in vivo acquisition. Stromal progenitor cells with this phenotype could have an osteoimmunological role during bone regeneration.
Mots-clé
Bone Marrow Cells/drug effects, Bone Marrow Cells/immunology, Bone Marrow Cells/metabolism, Fibroblast Growth Factor 2/immunology, Fibroblast Growth Factor 2/pharmacology, Gene Expression/drug effects, Gene Expression Profiling, HLA-DR Antigens/drug effects, HLA-DR Antigens/genetics, Humans, Interferon-gamma/immunology, Interferon-gamma/metabolism, Interferon-gamma/pharmacology, Interleukin-1beta/immunology, Interleukin-1beta/metabolism, Interleukin-1beta/pharmacology, Mesenchymal Stem Cells/drug effects, Mesenchymal Stem Cells/immunology, Mesenchymal Stem Cells/metabolism, Mitogen-Activated Protein Kinase Kinases/drug effects, Mitogen-Activated Protein Kinase Kinases/genetics, Mitogen-Activated Protein Kinase Kinases/metabolism, Osteoprotegerin/drug effects, Osteoprotegerin/genetics, Osteoprotegerin/metabolism, RANK Ligand/drug effects, RANK Ligand/genetics, RANK Ligand/metabolism, RNA, Messenger/genetics, RNA, Messenger/metabolism, Receptor Activator of Nuclear Factor-kappa B/drug effects, Receptor Activator of Nuclear Factor-kappa B/genetics, Reverse Transcriptase Polymerase Chain Reaction, Cytokines, Fibroblasts, Inflammation
Pubmed
Web of science
Open Access
Oui
Création de la notice
27/07/2020 17:56
Dernière modification de la notice
28/07/2020 5:26
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