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Origin and characterization of alpha smooth muscle actin-positive cells during murine lung development.
Moiseenko, Alena; Kheirollahi, Vahid; Chao, Cho-Ming; Ahmadvand, Negah; Quantius, Jennifer; Wilhelm, Jochen; Herold, Susanne; Ahlbrecht, Katrin; Morty, Rory E; Rizvanov, Albert A; Minoo, Parviz; El Agha, Elie; Bellusci, Saverio.
Afiliación
  • Moiseenko A; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Kheirollahi V; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Chao CM; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Ahmadvand N; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Quantius J; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Wilhelm J; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Herold S; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Ahlbrecht K; Department of Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, German Center for Lung Research (DZL), Bad Nauheim, Germany.
  • Morty RE; Department of Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, German Center for Lung Research (DZL), Bad Nauheim, Germany.
  • Rizvanov AA; Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
  • Minoo P; Department of Pediatrics, Division of Newborn Medicine, University of Southern California, Childrens Hospital Los Angeles, Los Angeles, California, USA.
  • El Agha E; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
  • Bellusci S; Excellence Cluster Cardio-Pulmonary System (ECCPS), Universities of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University Giessen, German Center for Lung Research (DZL), Giessen, Germany.
Stem Cells ; 35(6): 1566-1578, 2017 06.
Article en En | MEDLINE | ID: mdl-28370670
ACTA2 expression identifies pulmonary airway and vascular smooth muscle cells (SMCs) as well as alveolar myofibroblasts (MYF). Mesenchymal progenitors expressing fibroblast growth factor 10 (Fgf10), Wilms tumor 1 (Wt1), or glioma-associated oncogene 1 (Gli1) contribute to SMC formation from early stages of lung development. However, their respective contribution and specificity to the SMC and/or alveolar MYF lineages remain controversial. In addition, the contribution of mesenchymal cells undergoing active WNT signaling remains unknown. Using Fgf10CreERT2 , Wt1CreERT2 , Gli1CreERT2 , and Axin2CreERT2 inducible driver lines in combination with a tdTomatoflox reporter line, the respective differentiation of each pool of labeled progenitor cells along the SMC and alveolar MYF lineages was quantified. The results revealed that while FGF10+ and WT1+ cells show a minor contribution to the SMC lineage, GLI1+ and AXIN2+ cells significantly contribute to both the SMC and alveolar MYF lineages, but with limited specificity. Lineage tracing using the Acta2-CreERT2 transgenic line showed that ACTA2+ cells labeled at embryonic day (E)11.5 do not expand significantly to give rise to new SMCs at E18.5. However, ACTA2+ cells labeled at E15.5 give rise to the majority (85%-97%) of the SMCs in the lung at E18.5 as well as alveolar MYF progenitors in the lung parenchyma. Fluorescence-activated cell sorting-based isolation of different subpopulations of ACTA2+ lineage-traced cells followed by gene arrays, identified transcriptomic signatures for alveolar MYF progenitors versus airway and vascular SMCs at E18.5. Our results establish a new transcriptional landscape for further experiments addressing the function of signaling pathways in the formation of different subpopulations of ACTA2+ cells. Stem Cells 2017;35:1566-1578.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Actinas / Miocitos del Músculo Liso / Pulmón Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Stem Cells Año: 2017 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Actinas / Miocitos del Músculo Liso / Pulmón Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Stem Cells Año: 2017 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Reino Unido