Research Paper Volume 11, Issue 9 pp 2889—2897
c-Met as a new marker of cellular senescence
- 1 The Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, Beer Sheva, 8410501, Israel
Received: April 8, 2019 Accepted: May 4, 2019 Published: May 13, 2019
https://doi.org/10.18632/aging.101961How to Cite
Copyright: Boichuck et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Here, we reported for the first time an increased expression of c-Met protein in primary cultures of human dermal and pulmonary fibroblasts of late passages. This suggests that c-Met could serve as an early marker of cellular senescence (CS). The levels of c-Met-related signaling proteins phospho-Akt and Stat3 were also increased in (pre)senescent fibroblasts. Considering the anti-apoptotic activity of Akt and the involvement of Stat3 in mediating the effects of proinflammatory cytokines, the findings of this study indicate that c-Met could contribute through its downstream targets or partners to at least two major phenotypical features of CS – resistance to apoptosis and senescence-associated secretory phenotype.
Abbreviations
α-SMA: α-smooth muscle actin; BSA: bovine serum albumin; CS: cellular senescence; HGF: hepatocyte growth factor; PDT: population doubling time; SA-β-gal: senescence-associated β-galactosidase; SASP: senescence-associated secretory phenotype.