PhD Scientific Days 2025

Poster Session III. - K: Theoretical and Translational Medicine

The mechanosensory transient receptor potential vanilloid 4 mediates its effects through prostanoids in the urinary bladder

Előadó neve

Dr. Lénárt Ádám

Neptun code

WZU7TJ

Előadó munkahelye

Institute of Translational Medicine

Előadó telefonszáma

06306309988

Előadó e-mail címe

lenartadam15@gmail.com

Az előadás címe

The mechanosensory transient receptor potential vanilloid 4 mediates its effects through prostanoids in the urinary bladder

Szerző(k) neve és munkahelye

Ádám Lénárt¹, Kinga Borsodi¹, Helga Balla¹, Péter József Molnár², Bálint Dér², Péter Nyirády³, Zoltán Benyó¹

1: Institute of Translational Medicine
2: Institute of Translational Medicine, Department of Urology
3: Department of Urology

Bemutatás módja

Poszter

Szekció

Poster Session III. - K: Theoretical and Translational Medicine

Language of the presentation

English

Preferred session

Theoretical and Translational Medicine

Összefoglaló szövege

Introduction: Mechanotransduction, where ion channels sense bladder filling, is a key regulator of normal urinary bladder function. Upon reaching a certain wall tension, signaling pathways are activated, leading to the urge to urinate. The transient receptor potential vanilloid type 4 (TRPV4) channel is a major mechanosensory component in this process. Conditions like overactive bladder syndrome, characterized by frequent and urgent urination, are thought to involve altered mechanotransduction. However, the detailed mechanisms are still not fully understood. Our goal was to study TRPV4-mediated bladder signaling to identify possible new therapeutic targets.
Methods: Experiments were conducted on adult male and female wild-type and cyclooxygenase 1 knock-out (COX1-KO) mice. Bladder function was assessed in vivo by transurethral cystometry and ex vivo by myography. Mediator levels were measured using ELISA kits.
Results: TRPV4 activation significantly enhanced bladder activity, an effect almost entirely abolished by the non-selective COX inhibitor indomethacin both in vivo and ex vivo. In COX1-KO mice, the effect was partially reduced, while in the presence of a COX2 inhibitor, it was fully eliminated. Levels of Prostaglandin E2 and Thromboxane A2, both COX products, rose significantly 5 minutes after TRPV4 activation and further increased after 10 minutes.
Conclusions: TRPV4 activation in the bladder wall triggers inflammatory mediator production, leading to increased bladder excitability through mainly local processes. Both COX1 and COX2 enzymes contribute to mediator production. We identified a signaling pathway where multiple intervention points could reduce bladder overactivity. These findings may aid the development of more targeted therapies for functional urological conditions associated with bladder hyperactivity.
Support: Hungarian NRDIO K-112964, K-125174, K-135683, K-139230, and EFOP-3.6.3-VEKOP-16-2017-00009 grants, 2024-2.1.1-EKÖP

University

Semmelweis University

Supervisor

Prof Dr. Zoltán Benyó

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies after complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

8254

Start

14:18

End

14:24