Verteporfin as a Medical Treatment in Peyronie's Disease
Autor: | Ruud A. Bank, Daan C J Mohede, Igle J. de Jong, Mels F. van Driel |
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Přispěvatelé: | Restoring Organ Function by Means of Regenerative Medicine (REGENERATE), Groningen Kidney Center (GKC) |
Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
Pathology
medicine.medical_specialty Urology Endocrinology Diabetes and Metabolism 030232 urology & nephrology lcsh:Medicine Dermatology 03 medical and health sciences Behavioral Neuroscience PHOTODYNAMIC THERAPY 0302 clinical medicine Endocrinology Fibrosis medicine DUPUYTRENS Peyronie's Disease YAP Cascade LOXL2 biology business.industry lcsh:R Verteporfin lcsh:Other systems of medicine Macular degeneration lcsh:RZ201-999 medicine.disease INCREASED MORTALITY Psychiatry and Mental health Reproductive Medicine 030220 oncology & carcinogenesis biology.protein Peyronie's disease ACTA2 business Myofibroblast Immunostaining Peyronie’s Disease medicine.drug |
Zdroj: | Sexual Medicine, Vol 6, Iss 4, Pp 302-308 (2018) Sexual Medicine Sexual medicine, 6(4), 302-308. ELSEVIER SCI LTD |
ISSN: | 2050-1161 |
Popis: | 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. |
Databáze: | OpenAIRE |
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