Abstract

Deletion of the epidermal water/glycerol transporter aquaporin-3 (AQP3) in mice reduced superficial skin conductance by approximately 2-fold (Ma, T., Hara, M., Sougrat, R., Verbavatz, J. M., and Verkman, A. S. (2002) J. Biol. Chem. 277, 17147-17153), suggesting defective stratum corneum (SC) hydration. Here, we demonstrate significant impairment of skin hydration, elasticity, barrier recovery, and wound healing in AQP3 null mice in a hairless (SKH1) genetic background and investigate the cause of the functional defects by analysis of SC morphology and composition. Utilizing a novel (3)H(2)O distribution method, SC water content was reduced by approximately 50% in AQP3 null mice. Skin elasticity measured by cutometry was significantly reduced in AQP3 null mice with approximately 50% reductions in elasticity parameters Uf, Ue, and Ur. Although basal skin barrier function was not impaired, AQP3 deletion produced an approximately 2-fold delay in recovery of barrier function as measured by transepidermal water loss after tape stripping. Another biosynthetic skin function, wound healing, was also approximately 2-fold delayed by AQP3 deletion. By electron microscopy AQP3 deletion did not affect the structure of the unperturbed SC. The SC content of ions (Na(+), K(+), Ca(2+), Mg(2+)) and small solutes (urea, lactic acid, glucose) was not affected by AQP3 deletion nor was the absolute amount or profile of lipids and free amino acids. However, AQP3 deletion produced significant reductions in glycerol content in SC and epidermis (in nmol/microg protein: 5.5 +/- 0.4 versus 2.3 +/- 0.7 in SC; 0.037 +/- 0.007 versus 0.022 +/- 0.005 in epidermis) but not in dermis or blood. These results establish hydration, mechanical, and biosynthetic defects in skin of AQP3-deficient mice. The selective reduction in epidermal and SC glycerol content in AQP3 null mice may account for these defects, providing the first functional evidence for physiologically important glycerol transport by an aquaporin.

Highlights

  • Deletion of the epidermal water/glycerol transporter aquaporin-3 (AQP3) in mice reduced superficial skin conductance by ϳ2-fold

  • AQP3 is a water/glycerol transporter expressed in the basal layer of keratinocytes in mammalian epidermis

  • We find here that stratum corneum (SC) water and glycerol content are significantly reduced in AQP3 null mice, which as explained below probably accounts for the abnormalities in skin mechanical and biochemical functions

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Summary

Introduction

Deletion of the epidermal water/glycerol transporter aquaporin-3 (AQP3) in mice reduced superficial skin conductance by ϳ2-fold AQP3 deletion produced significant reductions in glycerol content in SC and epidermis (in nmol/␮g protein: 5.5 ؎ 0.4 versus 2.3 ؎ 0.7 in SC; 0.037 ؎ 0.007 versus 0.022 ؎ 0.005 in epidermis) but not in dermis or blood These results establish hydration, mechanical, and biosynthetic defects in skin of AQP3-deficient mice. We found significant reduction in SC water content in AQP3-deficient mice, as measured using a new 3H2O distribution method, as well as impairment in skin elasticity, barrier recovery, and wound healing. We propose that reduced glycerol transport across the AQP3-deficient epidermis lowers SC glycerol content and is responsible for the impairment in SC hydration, skin mechanical properties, and biosynthetic functions

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