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Low-dose calcipotriol can elicit wound closure, anti-microbial, and anti-neoplastic effects in epidermolysis bullosa keratinocytes.

EB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria. c.gruber@salk.at. EB House Austria, Research Program for Molecular Therapy of Genodermatoses, Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria. Experimental & Clinical Cell Therapy Institute, Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), PMU Salzburg, Salzburg, Austria. Institute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos #06-08, Singapore, Singapore. Skin Research Institute of Singapore, A*STAR, 8A Biomedical Grove, Immunos #06-06, Singapore, Singapore. University Clinic of Ophthalmology and Optometry, Research Program for Ophthalmology and Glaucoma Research, Paracelsus Medical University Salzburg, Salzburg, Austria. Landesapotheke Salzburg, Department of Production, Hospital Pharmacy, Salzburg, Austria. Department of Dermatology, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.

Scientific reports. 2018;(1):13430
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Abstract

Recessive dystrophic epidermolysis bullosa (RDEB) patients suffer from chronic and repeatedly infected wounds predisposing them to the development of aggressive and life-threatening skin cancer in these areas. Vitamin D3 is an often neglected but critical factor for wound healing. Intact skin possesses the entire enzymatic machinery required to produce active 1-alpha,25-dihydroxyvitamin D3 (calcitriol), underscoring its significance to proper skin function. Injury enhances calcitriol production, inducing the expression of calcitriol target genes including the antimicrobial peptide cathelicidin (hCAP18), an essential component of the innate immune system and an important wound healing factor. We found significantly reduced hCAP18 expression in a subset of RDEB keratinocytes which could be restored by calcipotriol treatment. Reduced scratch closure in RDEB cell monolayers was enhanced up to 2-fold by calcipotriol treatment, and the secretome of calcipotriol-treated cells additionally showed increased antimicrobial activity. Calcipotriol exhibited anti-neoplastic effects, suppressing the clonogenicity and proliferation of RDEB tumor cells. The combined wound healing, anti-microbial, and anti-neoplastic effects indicate that calcipotriol may represent a vital therapeutic option for RDEB patients which we could demonstrate in a single-patient observation study.