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Research Paper|Volume 7, Issue 12|pp 1185—1197

Knockout of Angiotensin AT2 receptors accelerates healing but impairs quality

Mahya Faghih1, Sayed M Hosseini2, Barbara Smith3, Amir Mehdi Ansari2, Frank Lay2, Ali Karim Ahmed2, Tedashi Inagami4, Guy P Marti2, John W Harmon2, Jeremy D Walston1, Peter M Abadir1
  • 1Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA
  • 2Department of Surgery and Hendrix Burn/Wound Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA
  • 3Cell Biology Imaging Facility, Johns Hopkins University School of Medicine Baltimore, MD 21224, USA
  • 4Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
Received: December 4, 2015Accepted: December 2, 2015Published: December 31, 2015
https://doi.org/10.18632/aging.100868

Copyright: © 2015 Faghih 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

Wounds are among the most common, painful, debilitating and costly conditions in older adults. Disruption of the angiotensin type 1 receptors (AT1R), has been associated with impaired wound healing, suggesting a critical role for AT1R in this repair process. Biological functions of angiotensin type 2 receptors (AT2R) are less studied. We investigated effects of genetically disrupting AT2R on rate and quality of wound healing. Our results suggest that AT2R effects on rate of wound closure depends on the phase of wound healing. We observed delayed healing during early phase of wound healing (inflammation). An accelerated healing rate was seen during later stages (proliferation and remodeling). By day 12, fifty percent of AT2R−/− mice had complete wound closure as compared to none in either C57/BL6 or AT1R−/− mice. There was a significant increase in AT1R, TGFβ1 and TGFβ2 expression during the proliferative and remodeling phases in AT2R−/− mice. Despite the accelerated closure rate, AT2R−/− mice had more fragile healed skin. Our results suggest that in the absence of AT2R, wound healing rate is accelerated, but yielded worse skin quality. Elucidating the contribution of both of the angiotensin receptors may help fine tune future intervention aimed at wound repair in older individuals