PhD Scientific Days 2022

Molecular Sciences III. (Poster discussion will take place on the terrace of the room during the Coffee Break)

Revealing the Intracellular Changes of ERK/MAPK, NF-κB and Wnt Signalling Pathways in K/BxN Treated Wild Type and ARHGAP25 Knock-out Mice

Előadó neve

Sasvári, Péter

Előadó munkahelye

Semmelweis University, Department of Physiology

Előadó telefonszáma

06309650396

Előadó e-mail címe

sasvari.peti@gmail.com

Az előadás címe

Revealing the Intracellular Changes of ERK/MAPK, NF-κB and Wnt Signalling Pathways in K/BxN Treated Wild Type and ARHGAP25 Knock-out Mice

Szerző(k) neve és munkahelye

Péter Sasvári1, Domonkos Czárán1, Roland Csépányi-Kömi1
1 Semmelweis University, Department of Physiology

Bemutatás módja

Poszter

Szekció

Molecular Sciences III. (Poster discussion will take place on the terrace of the room during the Coffee Break)

Language of the presentation

English

Preferred session

Molecular Sciences

Összefoglaló szövege

Rheumatoid arthritis is an autoimmune and inflammatory disease which is estimated to affect approximately one percent of the population. This long-term condition causes pain, swelling and stiffness usually in the joints which severely affects the patient’s life. Although the long-term complications can be reduced to some extent with the use of drug therapies, any new findings in this field can have an enormous effect on the treatment of said disease.
ARHGAP25 is a Rac specific GTPase protein (GAP) that is highly expressed in leukocytes and proved to be a relevant modulator of immune responses. Studies found that the absence of ARHGAP25 can alleviate the effect of K/BxN induced arthritis in knock-out (K.O.) mouse model.

We were curious to reveal the changes in different intracellular pathways that can take part in the development of the disease and see if we can find a change in protein expression in case of the absence of ARHGAP25.

We created an ARHGAP25 K.O. mouse strain and used the K/BxN arthritis model to see the effect of ARHGAP25 on the progression of the disease. K.O. and wild type (W.T.) mice were treated with either K/BxN or control (BxN) serum. On day 5, after scoring their hind paws we terminated the mice to use their ankle for Western Blot analysis. We examined 5 phospho- and 8 total protein content from the ERK/MAPK, NF-κB and Wnt signalling pathways and performed densitometry to evaluate the results. GAPDH content was used as loading control and clinical score as an indirect marker of inflammation.

The proteomic levels were characterised in each sample group (W.T. vs. K.O. and BxN vs. K/BxN). We detected changes in the content of most proteins due to the treatment with K/BxN serum. Some of them showed strong correlation with the clinical score which suggests their importance in the development. The effect of total ARHGAP25 deletion in the mouse strain appears to affect in some protein levels.

The K/BxN serum-transfer induced arthritis has a visible effect on the protein levels of different signalling pathways. Phosphorylation of certain proteins seems to have an important role in the progression of the disease and some protein levels might be affected by the absence of ARHGAP25.

Funding: János Bolyai Research Scholarship of the Hungarian Academy of Sciences, ÚNKP-20-5-SE-2, EFOP-3.6.3-VEKOP-16-2017-00009 and NKFIH FK_18/128376 grants.

University and Doctoral School

Semmelweis University, Doctoral School of Molecular Medicine

Supervisor

dr. Roland Csépányi-Kömi

Publication of my abstract

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

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

6060

Start

12:50

End

12:55

Authors (legacy)

Péter Sasvári1, Domonkos Czárán1, Roland Csépányi-Kömi1
1 Semmelweis University, Department of Physiology