Form of presentation | Articles in international journals and collections |
Year of publication | 2015 |
Язык | английский |
|
Beluchi Saverio , author
|
Bibliographic description in the original language |
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. |
Annotation |
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). |
Keywords |
Fibroblast growth factors, Lung epithelial cell |
The name of the journal |
Am J Physiol Lung Cell Mol Physiol
|
URL |
http://www.ncbi.nlm.nih.gov/pubmed/25820524 |
Please use this ID to quote from or refer to the card |
https://repository.kpfu.ru/eng/?p_id=113202&p_lang=2 |
Full metadata record |
Field DC |
Value |
Language |
dc.contributor.author |
Beluchi Saverio |
ru_RU |
dc.date.accessioned |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.available |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.issued |
2015 |
ru_RU |
dc.identifier.citation |
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. |
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/eng/?p_id=113202&p_lang=2 |
ru_RU |
dc.description.abstract |
Am J Physiol Lung Cell Mol Physiol |
ru_RU |
dc.description.abstract |
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). |
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
Fibroblast growth factors |
ru_RU |
dc.subject |
Lung epithelial cell |
ru_RU |
dc.title |
Attenuating endogenous Fgfr2b ligands during bleomycin-induced lung fibrosis does not compromise murine lung repair |
ru_RU |
dc.type |
Articles in international journals and collections |
ru_RU |
|