1 Ocak 2018 Dergi makalesi Açık Erişim

Cagnan, Ilgin; Gunel-Ozcan, Aysen; Aerts-Kaya, Fatima; Ameziane, Najim; Kuskonmaz, Baris; Dorsman, Josephine; Gumruk, Fatma; Uckan, Duygu

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    "creators": [
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        "affiliation": "Hacettepe Univ, Inst Hlth Sci, Dept Stem Cell Sci, Ctr Stem Cell Res & Dev, TR-06100 Ankara, Turkey", 
        "name": "Cagnan, Ilgin"
      }, 
      {
        "affiliation": "Hacettepe Univ, Inst Hlth Sci, Dept Stem Cell Sci, Ctr Stem Cell Res & Dev, TR-06100 Ankara, Turkey", 
        "name": "Gunel-Ozcan, Aysen"
      }, 
      {
        "affiliation": "Hacettepe Univ, Inst Hlth Sci, Dept Stem Cell Sci, Ctr Stem Cell Res & Dev, TR-06100 Ankara, Turkey", 
        "name": "Aerts-Kaya, Fatima"
      }, 
      {
        "affiliation": "Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, Amsterdam, Netherlands", 
        "name": "Ameziane, Najim"
      }, 
      {
        "affiliation": "Hacettepe Univ, Div Bone Marrow Transplantat Unit, Dept Pediat, Fac Med, Ankara, Turkey", 
        "name": "Kuskonmaz, Baris"
      }, 
      {
        "affiliation": "Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, Amsterdam, Netherlands", 
        "name": "Dorsman, Josephine"
      }, 
      {
        "affiliation": "Hacettepe Univ, Dept Pediat Hematol, Fac Med, Ankara, Turkey", 
        "name": "Gumruk, Fatma"
      }, 
      {
        "name": "Uckan, Duygu"
      }
    ], 
    "description": "Transforming growth factor beta (TGF-beta) secretion from cells in the bone marrow (BM) niche affects hematopoietic stem cell (HSC) fate and has a cardinal role in HSC quiescence. BM mesenchymal stem cells (BM-MSCs), a component of the BM niche, may produce abnormal levels of TGF-beta in Fanconi anemia (FA) and may play a role in bone marrow failure. Here, we molecularly and cellularly characterized FA BM-MSCs by addressing their immunophenotype, proliferation- and differentiation- capacity, reactive oxygen species (ROS) production, senescence activity as well as expression and secretion levels of TGF-beta isoforms. In ten FA patients, mutations were detected in FANCA (n = 7), FANCG (n = 1) and FANCD2 (n = 2) genes. The immunophenotype, with the exception of CD29, and differentiation capacity of FA BM-MSCs were similar to healthy donors. FA BM-MSCs showed decreased proliferation, increased ROS level and an arrest in G2 following DEB treatment. beta-galactosidase staining indicated elevated senescence of FANCD2-deficient cells. FA BM-MSCs displayed TGF-beta 1 mRNA levels similar to donor BM-MSCs, and was not affected by DEB treatment. However, secretion of TGF-beta was absent in FA-D2 BM-MSCs. Absence of TGF-beta secretion may be related to early onset of senescence of the FANCD2-deficient BM-MSCs. The proliferative response of FA-D2 BM-MSCs to rTGF-beta 1 was not different from FANCA-deficient and donor cells and raises the possibility that rTGF-beta 1 may reverse the senescence of the FANCD2-deficient BM-MSCs which needs to be investigated further.", 
    "doi": "10.1007/s12015-017-9794-5", 
    "has_grant": false, 
    "journal": {
      "issue": "3", 
      "pages": "425-437", 
      "title": "STEM CELL REVIEWS AND REPORTS", 
      "volume": "14"
    }, 
    "license": {
      "id": "cc-by"
    }, 
    "publication_date": "2018-01-01", 
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    "resource_type": {
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      "title": "Dergi makalesi", 
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    "title": "Bone Marrow Mesenchymal Stem Cells Carrying FANCD2 Mutation Differ from the Other Fanconi Anemia Complementation Groups in Terms of TGF-beta 1 Production"
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