Verteporfin as a Medical Treatment in Peyronie’s Disease

Daan C.J. Mohede, MD; Igle Jan de Jong, MD, PhD; Ruud A. Bank, PhD; Mels F. van Driel, MD, PhD

Sexual Medicine (Dec 2018)

Verteporfin as a Medical Treatment in Peyronie’s Disease

Daan C.J. Mohede, MD,
Igle Jan de Jong, MD, PhD,
Ruud A. Bank, PhD,
Mels F. van Driel, MD, PhD

Affiliations

Daan C.J. Mohede, MD: Department of Urology, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands; Corresponding Author: Daan C.J. Mohede, MD, University Medical Center Groningen, Department of Urology CB62, P.O. Box 30 001, 9700 RB Groningen, The Netherlands. Tel.: +31503613531; Fax: +31503619913
Igle Jan de Jong, MD, PhD: Department of Urology, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands
Ruud A. Bank, PhD: Department of Pathology & Medical Biology, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands
Mels F. van Driel, MD, PhD: Department of Urology, University of Groningen and University Medical Center Groningen, Groningen, the Netherlands

Journal volume & issue: Vol. 6, no. 4
pp. 302 – 308

Abstract

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Introduction: In Europe and the United States, verteporfin (Visudyne; VP) is registered and used in treating macular degeneration. Research showed that VP decreased expression of fibrotic genes in fibroblasts collected from nodules of patients suffering from Dupuytren’s disease, plausibly by de-activating transcription in the Yes Activated Protein (YAP) pathway. Aim: To analyze the effect of VP on myofibroblasts cultured from Peyronie’s disease (PD) plaques. Methods: At surgery for PD we took biopsies from the plaques of 5 patients. By immunostaining, the presence of the pathologic myofibroblasts was determined. After culturing cells, VP was dispensed in starvation medium for 24 and 48 hours and messenger(m)RNA levels of COL1A1, ACTA2, COL5A1, EDA-FN, LOXL2, CCN2, SERPINH1, PLOD2, and YAP were quantified and compared with controls with real-time polymerase chain reaction. Main Outcome Measure: mRNA-levels of COL1A1, ACTA2, COL5A1, EDA-FN, LOXL2, CCN2, SERPINH1, PLOD2, and YAP. Results: The pathologic phenotype of cells isolated from PD plaques was confirmed with baseline immunofluorescent stainings that showed considerable levels of α-smooth muscle actin, being a marker for the presence of myofibroblasts. The mRNA ratios of all the genes related to fibrosis (COL1A1, etc.) except YAP decreased significantly after treatment with VP within 24 and 48 hours. These results suggest inhibition of fibrosis in the YAP cascade, downstream of YAP. Conclusion: In our opinion, urologists must move the focus to disease before deformity, and the search for new oral or intralesional agents, well-tolerated and effective in both the acute and chronic phase of PD must continue. VP blocked the expression of genes related to fibrosis in the YAP cascade in myofibroblasts derived from PD plaque.Mohede DCJ, de Jong IJ, Bank RA, et al. Verteporfin as a medical treatment in Peyronie’s disease. Sex Med 2018;6:302–308. Key Words: Peyronie’s Disease, Verteporfin, Fibrosis, YAP Cascade

Published in Sexual Medicine

ISSN: 2050-1161 (Online)
Publisher: Oxford University Press
Country of publisher: United Kingdom
LCC subjects: Medicine
Website: https://academic.oup.com/smoa

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