title: [Trying to unravel an unresolved issue in regenerative medicine: gene expression profiling of MSCs].
abstract: BACKGROUND
  Mesenchymal stem cells (MSCs) are adult fibroblastoid progenitor cells. Because of their immunoregulatory properties and their so-called trophic effects, MSCs play an important role in tissue regeneration, inflammation and trauma. Tissue trauma and challenge, for example during radiotherapy or infection, result in the release of so-called "danger molecules", which may be derived from dying cells or incoming pathogens. The molecular response of MSCs to this tissue stress remains largely elusive.
  
  
  METHODS
  In this study we examined the cell biological response of MSCs derived from human parotid glands (pgMSCs) and used bacterial endotoxin as a model of tissue stress and inflammation. PgMSCs from 3 donors were isolated, expanded and tested for classical tri-lineage plus myogenic differentiation. The cell biological response to the model "stressor" endotoxin was examined by low density gene expression arrays.
  
  
  RESULTS
  Through immunofluorescence and immunohistochemistry we were able to proof osteogenic, adipogenic, chondrogenic, and myogenic differentiation potential characteristic for stem cells. In vitro, gene expression analysis showed a characteristic modulation of MSCs after stimulation with endotoxin Lipopolysaccharide (LPS). Specifically, receptors and ligands typically involved in immune regulation, such as interleukins, TGF-β, tumor necrosis factors (TNF), and toll-like receptors (TLR), were regulated.
  
  
  CONCLUSIONS
  Our study elucidates some key functions and molecules, which are regulated in MSCs during tissue stress and inflammation. A thorough understanding of their cell biological function will aid future rationale therapeutic application of MSCs.
authors.affiliation: University Hospital Bonn, ENT, Bonn. mark.jakob@ukb.uni-bonn.de
authors.forename: M
authors.initials: M
authors.lastname: Jakob
authors.forename: K
authors.initials: K
authors.lastname: Bruderek
authors.forename: F
authors.initials: F
authors.lastname: Bootz
authors.forename: S
authors.initials: S
authors.lastname: Lang
authors.forename: S
authors.initials: S
authors.lastname: Brandau
mesh_terms: D000328:Adult; D002454:Cell Differentiation / Q000235:genetics / Q000502:physiology; D005260:Female; D020869:Gene Expression Profiling / Q000379:methods*; D006801:Humans; D055261:Immunogenetic Phenomena / Q000235:genetics* / Q000276:immunology*; D066298:In Vitro Techniques; D007249:Inflammation / Q000235:genetics* / Q000276:immunology*; D018836:Inflammation Mediators / Q000502:physiology*; D007372:Interferons / Q000235:genetics / Q000502:physiology; D007378:Interleukins / Q000235:genetics / Q000502:physiology; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D059630:Mesenchymal Stem Cells / Q000378:metabolism*; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D010306:Parotid Gland / Q000166:cytology*; D044968:Regenerative Medicine / Q000379:methods*; D014022:Tissue Survival / Q000235:genetics* / Q000276:immunology*; D051193:Toll-Like Receptors / Q000235:genetics / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D007378:Interleukins; D008070:Lipopolysaccharides; D051193:Toll-Like Receptors; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons