Research Paper|Volume 7, Issue 3|pp 167—176

Wound healing and longevity: Lessons from long-lived αMUPA mice

Hagai Yanai¹, Dimitri Toren¹, Klemens Vierlinger², Manuela Hofner², Christa Nöhammer², Marco Chilosi³, Arie Budovsky¹, Vadim E. Fraifeld¹

¹The Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, Beer Sheva 84105, Israel
²AIT - Austrian Institute of Technology, ATU14703506, Vienna, Austria
³Department of Pathology, University of Verona, Verona, Italy

Received: January 18, 2015Accepted: February 21, 2015Published: February 24, 2015

https://doi.org/10.18632/aging.100726

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

Does the longevity phenotype offer an advantage in wound healing (WH)? In an attempt to answer this question, we explored skin wound healing in the long-lived transgenic αMUPA mice, a unique model of genetically extended life span. These mice spontaneously eat less, preserve their body mass, are more resistant to spontaneous and induced tumorigenesis and live longer, thus greatly mimicking the effects of caloric restriction (CR). We found that αMUPA mice showed a much slower age-related decline in the rate of WH than their wild-type counterparts (FVB/N). After full closure of the wound, gene expression in the skin of old αMUPA mice returned close to basal levels. In contrast, old FVB/N mice still exhibited significant upregulation of genes associated with growth-promoting pathways, apoptosis and cell-cell/cell-extra cellular matrix interaction, indicating an ongoing tissue remodeling or an inability to properly shut down the repair process. It appears that the CR-like longevity phenotype is associated with more balanced and efficient WH mechanisms in old age, which could ensure a long-term survival advantage.