Казанский (Приволжский) федеральный университет, КФУ
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ATTENUATING ENDOGENOUS FGFR2B LIGANDS DURING BLEOMYCIN-INDUCED LUNG FIBROSIS DOES NOT COMPROMISE MURINE LUNG REPAIR
Форма представленияСтатьи в зарубежных журналах и сборниках
Год публикации2015
Языканглийский
  • Белучи Саверио , автор
  • Библиографическое описание на языке оригинала MacKenzie B. Attenuating endogenous Fgfr2b ligands during bleomycin-induced lung fibrosis does not compromise murine lung repair / B. MacKenzie, I. Henneke, S. Hezel, D. Al Alam, E. El Agha, C.M. Chao, J. Quantius, J. Wilhelm, M. Jones, K. Goth, X. Li, W. Seeger, M. Königshoff, S. Herold, A.A. Rizvanov, A. Günther, S. Bellusci // American Journal of Physiology. - Lung Cellular and Molecular Physiology. – 2015. – Vol.308 (10). – P.L1014-L1024.
    Аннотация Fibroblast growth factors (Fgfs) mediate organ repair. Lung epithelial cell overexpression of Fgf10 postbleomycin injury is both protective and therapeutic, characterized by increased survival and attenuated fibrosis. Exogenous administration of FGF7 (palifermin) also showed prophylactic survival benefits in mice. The role of endogenous Fgfr2b ligands on bleomycin-induced lung fibrosis is still elusive. This study reports the expression of endogenous Fgfr2b ligands, receptors, and signaling targets in wild-type mice following bleomycin lung injury. In addition, the impact of attenuating endogenous Fgfr2b-ligands following bleomycin-induced fibrosis was tested by using a doxycycline (dox)-based inducible, soluble, dominant-negative form of the Fgfr2b receptor. Double-transgenic (DTG) Rosa26(rtTA/+);tet(O)solFgfr2b mice were validated for the expression and activity of soluble Fgfr2b (failure to regenerate maxillary incisors, attenuated recombinant FGF7 signal in the lung).
    Ключевые слова Fibroblast growth factors, Lung epithelial cell
    Название журнала Am J Physiol Lung Cell Mol Physiol
    URL http://www.ncbi.nlm.nih.gov/pubmed/25820524
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