MP36-07 UNDERSTANDING THE EFFECTS OF ACTINIDIN AS A COLLAGENASE ACTING TO TREAT HUMAN PEYRONIE’S DISEASE CELLS
Bibliographic record
Abstract
You have accessJournal of UrologyCME1 Apr 2023MP36-07 UNDERSTANDING THE EFFECTS OF ACTINIDIN AS A COLLAGENASE ACTING TO TREAT HUMAN PEYRONIE’S DISEASE CELLS Kevin Feng, Wongsakorn Kiattiburut, Duane Hickling, Jeremy Burton, and Jeffrey Campbell Kevin FengKevin Feng More articles by this author , Wongsakorn KiattiburutWongsakorn Kiattiburut More articles by this author , Duane HicklingDuane Hickling More articles by this author , Jeremy BurtonJeremy Burton More articles by this author , and Jeffrey CampbellJeffrey Campbell More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003270.07AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Peyronie’s Disease (PD) is a penile connective tissue disorder that affects approximately 10% of men. The collagenous plaques that hallmark the disease can result in penile curvature, painful erections, and/or erectile dysfunction. Intralesional injection of collagenase Clostridium histolyticum is the only FDA approved treatment for PD, however, is no longer available in Canada. The enzyme actinidin has the ability to hydrolyze collagen and fibrinogen. Our preliminary work has evaluated actindin on in vitro cellular PD models. Our objectives are to determine the mechanism by which actinidin can reduce collagen composition of in vitro human PD models and explore the cytotoxicity and gene expression of cells treated with actinidin. METHODS: Three human PD tissue groups were isolated for fibroblast cells and cultured using complete media. The cells were plated on a 96-well plate and treated with their respective treatments: media, saline, verapamil, actinidin at 50, 25 and 10 mg/ml for 24 hours. MTT assay, immunofluorescent staining, qPCR and collagen quantification assay were used to examine cellular cytotoxicity, cellular organization/morphology, and gene expression, respectively. Statistical analyses were employed using Python 3 and Prism 10. RESULTS: Actinidin significantly reduced the amount of cellular-bound collagen (p<0.01) in our human PD model. The immunofluorescent staining of smooth muscle actin showed a significant increase of normalized actin stained signal, suggesting possible compromise of the cell membrane of PD cells. Microscopic observation of cellular morphology demonstrated the increases of interstitial space in the actinidin treated group compared to negative control, indicating the alteration of extra cellular matrix. MTT assay demonstrated that high concentration of actinidin reduced cellular viability of the PD cells. CONCLUSIONS: Our preliminary study suggests the possible effects of actinidin in breaking down PD plaques by compromising the extracellular matrix, membrane-bound proteins, and the cellular membrane of human PD fibroblasts. An increased level of normalized actin in the high concentration actinidin group acts suggests a compromised plasma membrane and a potential mechanism of action. Further studies will investigate the optimal actinidin concentration that can safely reduce the collagen composition of human PD plaques. In the absence of durable FDA-approved treatments for PD in Canada, this novel option could offer future treatment potential. Source of Funding: Canadian Urology Association Scholarship Foundation - Canadian Mens Sexual Health Council © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e481 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Kevin Feng More articles by this author Wongsakorn Kiattiburut More articles by this author Duane Hickling More articles by this author Jeremy Burton More articles by this author Jeffrey Campbell More articles by this author Expand All Advertisement PDF downloadLoading ...
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".