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Título: | Lung regeneration after toxic injury is improved in absence of dioxin receptor |
Autor: | Morales-Hernández, Antonio; Nacarino-Palma, Ana; Moreno-Marín, Nuria; Barrasa, Eva; Paniagua-Quiñones, Beroé; Catalina-Fernández, Inmaculada; Alvarez-Barrientos, Alberto; Bustelo, Xosé R. CSIC ORCID ; Merino, Jaime; Fernández-Salguero, Pedro M. CSIC ORCID | Palabras clave: | Stemness Pluripotency Dioxin receptor Liver and lung regeneration |
Fecha de publicación: | 2017 | Editor: | Elsevier | Citación: | Stem Cell Research 25: 61-71 (2017) | Resumen: | Recent experimental evidences from cellular systems and from mammalian and non-mammalian animal models highlight novel functions for the aryl hydrocarbon/dioxin receptor (AhR) in maintaining cell differentiation and tissue homeostasis. Notably, AhR depletion stimulates an undifferentiated and pluripotent phenotype likely associated to a mesenchymal transition in epithelial cells and to increased primary tumorigenesis and metastasis in melanoma. In this work, we have used a lung model of epithelial regeneration to investigate whether AhR regulates proper tissue repair by adjusting the expansion of undifferentiated stem-like cells. AhR-null mice developed a faster and more efficient repair of the lung bronchiolar epithelium upon naphthalene injury that required increased cell proliferation and the earlier activation of stem-like Clara, Basal and neuroepithelial cells precursors. Increased basal content in multipotent Sca1/CD31/CD4 cells and in cells expressing pluripotency factors NANOG and OCT4 could also improve re-epithelialization in AhR-null lungs. The reduced response of AhR-deficient lungs to Sonic Hedgehog (Shh) repression shortly after injury may also help their improved bronchiolar epithelium repair. These results support a role for AhR in the regenerative response against toxins, and open the possibility of modulating its activation level to favor recovery from lesions caused by environmental contaminants. | Versión del editor: | https://doi.org/10.1016/j.scr.2017.10.009 | URI: | http://hdl.handle.net/10261/169146 | DOI: | 10.1016/j.scr.2017.10.009 | Identificadores: | doi: 10.1016/j.scr.2017.10.009 e-issn: 1876-7753 issn: 1873-5061 |
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