PhD Scientific Days 2026

Molecular Medicine 2.

ARHGAP25 regulates hematopoietic cell-dependent inflammation in the imiquimod-induced psoriasiform dermatitis model

Előadó neve

Ms. Bíró, Renáta

Neptune code

V38LNC

Előadó munkahelye

Department of Physiology,Semmelweis University, Budapest, Hungary

Előadó telefonszáma

06302343590

Előadó e-mail címe

biro.renata@phd.semmelweis.hu

Az előadás címe

ARHGAP25 regulates hematopoietic cell-dependent inflammation in the imiquimod-induced psoriasiform dermatitis model

Szerző(k) neve és munkahelye

Renáta Bíró¹, Péter Sasvári², Domonkos Czárán², Roland Csépányi-Kömi²

1: Department of Physiology,Semmelweis University, Budapest, Hungary
2: Department of Physiology, Semmelweis University, Budapest, Hungary

Bemutatás módja

Szóbeli

Szekció

Molecular Medicine 2.

Language of the presentation

Hungarian

Preferred session

Molecular Medicine

Összefoglaló szövege

Background: ARHGAP25 is a leukocyte-specific GTPase-activating protein that plays an important role in the regulation of immune cell function and inflammatory responses. Psoriasis is a chronic immune-mediated skin disease with a complex and not yet fully understood pathogenesis. Given the regulatory role of ARHGAP25 in inflammation, it may also contribute to the development and severity of psoriatic skin inflammation.
Aims: This study aimed to investigate the role of ARHGAP25 in the pathogenesis of psoriasis using the imiquimod (IMQ)-induced psoriasiform mouse model, with particular focus on disease severity and the contribution of hematopoietic cells.
Methods: The experiments were performed using wild-type (WT), ARHGAP25-deficient (KO), and bone marrow chimeric (WT→WT, KO→WT,WT→KO, KO→KO) mice were used in our experiments. Psoriasiform inflammation was induced by daily topical IMQ treatment for 6 consecutive days, while control animals received Vaseline. Disease progression was monitored by measuring skin thickness and scoring erythema, scaling, and induration. Following the treatment period, animals were further monitored for an additional 10–11 days to assess the resolution phase. To evaluate immune cell infiltration, skin samples were collected on days 4, 6, and 10. Infiltration was analyzed by flow cytometry and hematoxylin and eosin staining, and quantitative PCR (qPCR) analyses are planned to determine the expression of inflammatory markers.
Results: IMQ treatment induced pronounced inflammation in all experimental groups. ARHGAP25-deficient mice exhibited more severe clinical symptoms compared to WT animals, reflected by increased erythema and scaling scores. These findings were partially recapitulated in bone marrow chimeric mice, suggesting that hematopoietic cells contribute to the observed phenotype. Ongoing analyses of skin-infiltrating immune cells are expected to provide further insight into the cellular mechanisms underlying these differences.
Conclusions: Our results suggest that ARHGAP25 plays an anti-inflammatory role in the IMQ-induced psoriasiform dermatitis model, at least in part through hematopoietic cell-dependent mechanisms.
Funding: FK_18 128376, TKP2021-EGA-24

University

Semmelweis University

Supervisor

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

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

9137

Start

11:45

End

11:55