Epithelial-to-mesenchymal transition induces cell cycle arrest and parenchymal damage in renal fibrosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-09

AUTHORS

Sara Lovisa, Valerie S LeBleu, Björn Tampe, Hikaru Sugimoto, Komal Vadnagara, Julienne L Carstens, Chia-Chin Wu, Yohannes Hagos, Birgitta C Burckhardt, Tsvetelina Pentcheva-Hoang, Hersharan Nischal, James P Allison, Michael Zeisberg, Raghu Kalluri

ABSTRACT

Kidney fibrosis is marked by an epithelial-to-mesenchymal transition (EMT) of tubular epithelial cells (TECs). Here we find that, during renal fibrosis, TECs acquire a partial EMT program during which they remain associated with their basement membrane and express markers of both epithelial and mesenchymal cells. The functional consequence of the EMT program during fibrotic injury is an arrest in the G2 phase of the cell cycle and lower expression of several solute and solvent transporters in TECs. We also found that transgenic expression of either Twist1 (encoding twist family bHLH transcription factor 1, known as Twist) or Snai1 (encoding snail family zinc finger 1, known as Snail) expression is sufficient to promote prolonged TGF-β1-induced G2 arrest of TECs, limiting the cells' potential for repair and regeneration. In mouse models of experimentally induced renal fibrosis, conditional deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition of the EMT program and the maintenance of TEC integrity, while also restoring cell proliferation, dedifferentiation-associated repair and regeneration of the kidney parenchyma and attenuating interstitial fibrosis. Thus, inhibition of the EMT program in TECs during chronic renal injury represents a potential anti-fibrosis therapy. More... »

PAGES

998-1009

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm.3902

DOI

http://dx.doi.org/10.1038/nm.3902

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1018567687

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26236991


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