Yiwei Wang¹, Brenton R Condor², Brian Lesmana³, Roxanne Parungao⁴, Franica Garces Suarez⁵, Zhe Li⁶, Ulla Simanainen⁷, David Handelsman⁸ , Mark Cooper⁹ and Peter Maitz¹⁰

¹Burns Research, ANZAC Research Institute, The University of Sydney, NSW, 2137; yiweiwang@anzac.edu.au
²Burns Research, ANZAC Research Institute, The University of Sydney, NSW, 2137; bcon5353@uni.sydney.edu.au
³Burns Research, ANZAC Research Institute, The University of Sydney, NSW, 2137; bles5603@uni.sydnedy.edu.au
⁴Burns Research, ANZAC Research Institute, The University of Sydney, NSW, 2137; rpar4161@uni.sydney.edu.au
⁵Burns Research, ANZAC Research Institute, The University of Sydney, NSW, 2137; francia.suarez@sydney.edu.au
⁶Burns Unit, Concord Repatriation General Hospital, Concord, NSW, 2137; zhe.li@sswahs.nsw.gov.au
⁷Andrology, ANZAC Research Institute, The University of Sydney, NSW, 2137; usimanainen@anzac.edu.au
⁸Andrology, ANZAC Research Institute, The University of Sydney, NSW, 2137; djh@anzac.edu.au
⁹Adrenal Steroid, ANZAC Research Institute, The University of Sydney, NSW, 2137; mark.cooper@sydney.edu.au
¹⁰Burns Unit, Concord Repatriation General Hospital, Concord, NSW, 2137; Burns Research, ANZAC Research Institute, ¹¹The University of Sydney, NSW, 2137; peter.maitz@sydney.edu.au

Rational

Androgens, acting via androgen receptor (AR), inhibit cutaneous wound repair in men and male mice. In contrast, recent clinical studies have reported that testosterone and an androgen analog (Oxandrolone) promotes healing of burn injuries. This finding points to a contradictory and context-dependent role of androgens in wound healing that differ between burn injury and simple incisional skin wound healing.

Objective

The aim of this study was to investigate how AR-mediated androgen actions modify the complex burn injury wound healing.

Methods

A mouse burn injury model was established to create the accompanying hypermetabolic-catabolic state. Mice were subjected to a thermal injury from a hot brass rod (4cm2) constituting a severe large burn. After 48 hrs following thermal injury, the wound site was debrided to remove damaged skin and to avoid infection prior to wound dressing. Following the injuries, mice were weighed daily, and metabolic changes, lean mass and muscle wasting were assessed to determine if androgens via AR modify the catabolic state that develops after burns injury. Wound healing rate, epidermal migration and healing processes were also analysed.

Results

Our preliminary study showed that burn wounds in all mice caused systemic hypermetabolism syndrome and continued weight lost and muscle wasting over 7 days. We found that androgens acting via AR significantly promote wound healing post thermal injury. In AR knockout mice, burn wound repair was markedly delayed with ~70% wound area remaining unhealed after 7 days compared to wild type mice. Moreover, AR knock out significantly reduced re-epithelialisation with very limited keratinocytes proliferation.

Key Words 

Androgens, burn injury, wound healing, mouse model

Biography

Dr Yiwei Wang is a research fellow at the ANZAC Research Institute at Concord Hospital. She studied her Pharmacy degree at China Pharmaceutical University and obtained her PhD from Kingston University, United Kingdom in November 2007.  Her initial work focused on the production of a new biomaterial scaffold which was used for controlled drug delivery and tissue engineering. In 2010, she joined the newly established Burns Research group in the ANZAC Research Institute as an expert specializing in wound healing and skin regeneration. She is now leading a group of researchers looking at regulation of steroid in burn injury.