PhD Scientific Days 2024

Poster Session K - Theoretical and Translational Medicine 2.

Angiotensin II-Driven Systemic Inflammation Enhances C3a-Induced Vasoconstriction in Murine Models

Előadó neve

Dr. Babay, Imre

Neptun code

VATYPV

Előadó munkahelye

Institute of Translational Medicine, Semmelweis University

Előadó telefonszáma

+36302166037

Előadó e-mail címe

imibabay@gmail.com

Az előadás címe

Angiotensin II-Driven Systemic Inflammation Enhances C3a-Induced Vasoconstriction in Murine Models

Szerző(k) neve és munkahelye

Imre Babay¹, Nóra Melinda Kerkovits¹, Csillag Virág Tóth¹, Balázs Besztercei¹, Mónika Kosztelnik^1,2, Zoltán Benyó^1,2

1: Institute of Translational Medicine, Semmelweis University
2: HUN-REN-SE Cerebrovascular and Neurocognitive Disease Research Group, Semmelweis University

Bemutatás módja

Poszter

Szekció

Poster Session K - Theoretical and Translational Medicine 2.

Language of the presentation

English

Preferred session

Theoretical and Translational Medicine

Összefoglaló szövege

Introduction: Our previous research has shown that the C3a receptor (C3aR) has been identified in various cell types within the mouse aortic wall, and our results indicate that the vasoconstrictive effect of the C3a anaphylatoxin is mediated by adventitial cells, likely macrophages.

Aims: This study aimed to explore the impact of chronic angiotensin II (Ang II) administration, a model of systemic inflammation, on C3a-induced vasoconstriction.

Method: Isometric tension changes in aortic segments of adult male C57BL/6 mice were measured using myography. Ang II or saline was delivered via osmotic pumps for two weeks at a dosage of 520 ng/kg/min. Gene expression levels of the C3AR1 anaphylatoxin receptor and macrophage markers (F4/80, CD68) in the aortic segments were quantified using real-time PCR. The localization of C3AR1 was confirmed via immunohistochemistry, and C3AR1 protein levels were quantified by Western blot analysis.

Results: Aortic segments from Ang II-treated mice demonstrated increased responsiveness to C3a compared to controls. Ang II infusion led to an upregulation of C3AR1 and macrophage marker expression, especially in the adventitia. Endothelium removal enhanced, whereas adventitia removal abolished, C3a-induced vasoconstriction. The response to C3a was also abolished by inhibitors of cyclooxygenase (COX) and thromboxane prostanoid (TP) receptors.

Conclusion: Our findings suggest that systemic inflammation amplifies C3a-induced vasoconstriction, mediated by thromboxane A2 release from adventitial macrophages. Targeting C3AR or TP receptors may be a promising therapeutic strategy to mitigate vascular dysfunction in systemic inflammatory diseases.

Funding: EFOP-3.6.3-VEKOP-16-2017-00009, OTKA K-139230, 2020-1.1.6-JÖVŐ-2021-00010, RRF-2.1.2.-12-2022-0001, and TKP2021-EGA-25.

University

Semmelweis University

Supervisor

Zoltán Benyó

Publication of my abstract

I 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

6957

Start

16:35

End

16:38