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Verteporfin as a Medical Treatment in Peyronie’s Disease
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-acti...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302152/ https://www.ncbi.nlm.nih.gov/pubmed/30274909 http://dx.doi.org/10.1016/j.esxm.2018.08.002 |
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author | Mohede, Daan C.J. de Jong, Igle Jan Bank, Ruud A. van Driel, Mels F. |
author_facet | Mohede, Daan C.J. de Jong, Igle Jan Bank, Ruud A. van Driel, Mels F. |
author_sort | Mohede, Daan C.J. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6302152 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-63021522018-12-21 Verteporfin as a Medical Treatment in Peyronie’s Disease Mohede, Daan C.J. de Jong, Igle Jan Bank, Ruud A. van Driel, Mels F. Sex Med Peyronie's Disease 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. Elsevier 2018-09-28 /pmc/articles/PMC6302152/ /pubmed/30274909 http://dx.doi.org/10.1016/j.esxm.2018.08.002 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Peyronie's Disease Mohede, Daan C.J. de Jong, Igle Jan Bank, Ruud A. van Driel, Mels F. Verteporfin as a Medical Treatment in Peyronie’s Disease |
title | Verteporfin as a Medical Treatment in Peyronie’s Disease |
title_full | Verteporfin as a Medical Treatment in Peyronie’s Disease |
title_fullStr | Verteporfin as a Medical Treatment in Peyronie’s Disease |
title_full_unstemmed | Verteporfin as a Medical Treatment in Peyronie’s Disease |
title_short | Verteporfin as a Medical Treatment in Peyronie’s Disease |
title_sort | verteporfin as a medical treatment in peyronie’s disease |
topic | Peyronie's Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302152/ https://www.ncbi.nlm.nih.gov/pubmed/30274909 http://dx.doi.org/10.1016/j.esxm.2018.08.002 |
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