PhD Scientific Days 2025

Poster Session II. - B: Molecular Medicine

ARHGAP25 has an anti-inflammatory role in the imiquimod-induced psoriasis mouse model

Előadó neve

Bíró Renáta, PhD

Neptun code

V38LNC

Előadó munkahelye

Semmelweis University Institute of Physiology

Előadó telefonszáma

+36-30/23-43-590

Előadó e-mail címe

biro.renata@phd.semmelweis.hu

Az előadás címe

ARHGAP25 has an anti-inflammatory role in the imiquimod-induced psoriasis mouse model

Szerző(k) neve és munkahelye

Renáta Bíró PhD¹, Péter Sasvári¹, Dr. Roland Csépányi-Kömi¹

1: Semmelweis University Institute of Physiology

Bemutatás módja

Poszter

Szekció

Poster Session II. - B: Molecular Medicine

Language of the presentation

Hungarian

Preferred session

Molecular Medicine

Összefoglaló szövege

Background: ARHGAP25 is a leukocyte-specific GTPase-activating protein that regulates immune cell functions and inflammation. Psoriasis is a common autoimmune skin disease with a complex, partly unclear pathogenesis. Due to its regulatory role, ARHGAP25 may contribute to psoriasis development.
Aims: This research project aims to investigate the role of ARHGAP25 in the pathomechanism of psoriasis.
Methods: We used Arhgap25+/+ (WT), Arhgap25-/- (KO), bone marrow chimeric (WT→WTCD45.1, KO→WTCD45.1), and reverse bone marrow chimeric (WTCD45.1→KO, WTCD45.1→WT) mouse strains. The psoriasiform inflammation on the skin was induced by daily Imiquimod (IMQ) application, and vaseline was used as control. The backs of the mice were shaved, and the progression of the inflammation was monitored for 6 days by measuring the double skin thickness and scoring the main visible symptoms of the inflammation (desquamation, induration, and erythema). On day 6, spleens were excised, measured, and lysed for leukocyte counting.
Results: IMQ treatment induced inflammation in WT and KO groups, with comparable increase in skin thikness. However, KO mice displayed more severe clinical symptoms, with significantly higher erythema scores from day 3 and increased desquamation scores on days 4 and 6. In bone marrow chimeras, the results closely mirrored our previously mentioned findings. Mice receiving KO hematopoietic cells on a WT background exhibited increased skin thickness and elevated clinical scores, indicating a stronger inflammatory response. Additionally, a significant increase in spleen size was observed in this group. In reverse chimeras no clear difference in inflammatory response has been observed. However, in contrast to the normal chimera results, splenomegaly was less severe in WTCD45.1→KO mice.
Conclusions: Previously, we found that ARHGAP25-deficiency mitigates the symptoms of autoantibody-induced arthritis. In this project, we successfully applied the IMQ-induced psoriasis model and, interestingly, observed more severe symptoms of inflammation upon ARHGAP25 deletion. This phenomenon was reproduced in bone marrow chimeras, suggesting a leukocyte-mediated explanation. However, further experiments are needed to better understand the underlying mechanisms.
Funding: EFOP-3.6.3-VEKOP-16-2017-00009, NKFIH FK_18/128376, TKP2021_EGA_24

University

Semmelweis University

Supervisor

Dr. Roland Csépányi-Kömi

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies before complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

9137

Start

18:06

End

18:12