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Study of SMAD-Dependent Signal Pathway in the Development of Early Pulmonary Fibrosis in Mice Infected with Influenza A/H1N1 Virus

tetano

Editor, Senior Moderator
Bull Exp Biol Med. 2017 Mar 30. doi: 10.1007/s10517-017-3678-1. [Epub ahead of print]
[h=1]Study of SMAD-Dependent Signal Pathway in the Development of Early Pulmonary Fibrosis in Mice Infected with Influenza A/H1N1 Virus.[/h] Shatskaya EV[SUP]1[/SUP], Kovner AV[SUP]2[/SUP], Potapova OV[SUP]2[/SUP], Cherdantseva LA[SUP]2[/SUP], Shkurupy VA[SUP]2[/SUP], Shestopalov AM[SUP]2[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] Early fibrosis of the visceral organs is one of the main complications of infection caused by influenza A virus. Structural manifestations and molecular regulators of the epithelialmesenchymal transformation as a possible mechanism of fibrosis progression were studied in mice infected with influenza A/H1N1 A/Tomsk/13/2010 virus. We found early fibrosis of the lungs against the background of minor changes in fibroblast count. However, enhanced expression of TGF-β and SMAD-2 by macrophages and alveolocytes attested to possible development of epithelial-mesenchymal transformation and its contribution to activation of fibrogenesis process in the lungs.


[h=4]KEYWORDS:[/h] SMAD-2; epithelial-mesenchymal transformations; fibrosis; influenza A/H1N1 A/Tomsk/13/2010 virus; lungs

PMID: 28361411 DOI: 10.1007/s10517-017-3678-1
 
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