The transcriptional signatures of cells from the human Peyronie's disease plaque and the ability of these cells to generate a plaque in a rat model suggest potential therapeutic targets
Gelfand RA., Vernet D., Kovanecz I., Rajfer J., Gonzalez-Cadavid NF.
Animal Study, published in J Sex Med (2015) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Sex Med (2015)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 25496134
- PMCID
- PMC4339076
- DOI
- 10.1111/jsm.12760
- Citations
- 20
Abstract (original English)
Introduction The success of medical therapies for Peyronie's disease (PD) has not been optimal, possibly because many of them went directly to clinical application without sufficient preclinical scientific research. Previous studies revealed cellular and molecular pathways involved in the formation of the PD plaque and in particular the role of the myofibroblast. Aims The current work aimed to determine under normal and fibrotic conditions what differentiates PD cells from tunica albuginea (TA) and corpora cavernosa (CC) cells by defining their global transcriptional signatures and testing in vivo whether PD cells can generate a PD-like plaque. Methods Human TA, PD, and CC cells were grown with transforming growth factor beta 1 (TGFβ1; TA+, PD+, CC+) or without it (TA-, PD-, CC-) and assayed by (i) immunofluorescence, Western blot and RT-PCR for myofibroblast, smooth muscle cell and stem cell markers; (ii) collagen content; and (iii) DNA microarray analysis. The ability of PD+ cells to induce a PD-like plaque in an immuno-suppressed rat model was assessed by Masson trichrome and Picrosirius Red stainings. Main outcomes measures Fibroproliferative features of PD cells and identification of related key genes as novel targets to reduce plaque size. Results Upon TGFβ1stimulation, collagen levels were increased by myofibroblasts in the PD+ but not in the CC+ cells. The transcription
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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