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Research Paper|Volume 7, Issue 9|pp 664—672

Cellular senescence-like features of lung fibroblasts derived from idiopathic pulmonary fibrosis patients

Hagai Yanai1, Albert Shteinberg1, Ziv Porat2, Arie Budovsky1,3, Alex Braiman1, Rolf Zeische4, Vadim E. Fraifeld1
  • 1The Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva 84105, Israel
  • 2Flow Cytometry Unit, Department of Biological services, Weizmann Institute of Science, Rehovot 76100, Israel
  • 3Judea Regional Research & Development Center, Carmel 90404, Israel
  • 4Division of Pulmonary Medicine, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria

* * Equal contribution

Received: August 9, 2015Accepted: September 12, 2015Published: September 22, 2015
https://doi.org/10.18632/aging.100807

Copyright: © 2015 Yanai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Idiopathic pulmonary fibrosis (IPF) is an age-related fatal disease with unknown etiology and no effective treatment. In this study, we show that primary cultures of fibroblasts derived from lung biopsies of IPF patients exhibited (i) accelerated replicative cellular senescence (CS); (ii) high resistance to oxidative-stress-induced cytotoxicity or CS; (iii) a CS-like morphology (even at the proliferative phase); and (iv) rapid accumulation of senescent cells expressing the myofibroblast marker α-SMA. Our findings suggest that CS could serve as a bridge connecting lung aging and its quite frequent outcome -- pulmonary fibrosis, and be an important player in the disease progression. Consequently, targeting senescent cells offers the potential of being a promising therapeutic approach.