PhD Scientific Days 2025

Poster Session III. - K: Theoretical and Translational Medicine

Vasoactive Effects of Lysophosphatidic Acid in Murine Pulmonary Arteries

Előadó neve

Mr. Varga Tamás

Neptun code

RMRLGF

Előadó munkahelye

Institute of Translational Medicine

Előadó telefonszáma

+36205158141

Előadó e-mail címe

changchoina@gmail.com

Az előadás címe

Vasoactive Effects of Lysophosphatidic Acid in Murine Pulmonary Arteries

Szerző(k) neve és munkahelye

Tamás Varga¹, Anna Monori-Kiss¹, Éva Ruisanchez¹, Bence Varga¹, Zoltán Benyó¹

1: Institute of Translational Medicine

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: Lysophosphatidic acids (LPA) comprise a lipid mediator family with various vascular effects that they elicit via six specific, G-protein coupled receptors (LPAR1-6). Its dual vasoconstrictive and vasodilatative effects are thoroughly studied in murine aorta, where the polyunsaturated LPA species, among them the linoleoyl or 18:2 LPA, which is the most abundant LPA species in plasma, cause a NO-dependent decrease, and a prostanoid-dependent increase in vascular tone.
Aims: The investigation of the effects of 18:2 LPA on murine vascular tone, and the signal transduction pathways involved.
Methods: The vascular tone of the left and right extralobar pulmonary arteries prepared from C57Bl/6 mice was measured with wire myography. The investigation of the signal transduction pathways was carried out with pharmacological inhibitors, including the LPAR1/3 blocker Ki16425, the thromboxane prostanoid receptor antagonist SQ29548, and the non-selective nitric oxide synthase inhibitor l-NAME.
Results: 18:2 LPA caused significant vasoconstriction, but no vasodilation, in the murine pulmonary arteries. The effect was found to be independent of age, gender, and endothelial function. The response could be moderately augmented by phenylephrine induced precontraction. Ki16425 completely abolished LPA-induced vasoconstriction, whereas SQ29548 failed to alter it.
Conclusion: In murine pulmonary arteries, 18:2 LPA elicits a significant vasoconstrictive response without vasodilation. The receptor responsible for the effect might be LPAR1 or LPAR3, and the vasoconstriction is not mediated by the prostanoid pathway. The results, which point to basic differences compared to the LPA effects seen in murine aorta, implicate 18:2 LPA as a potential regulator of pulmonary circulation under physiological and pathophysiological conditions.
Funding: NRDN grants K-125174, K-135683, K-139230, Advanced-151053 and TKP 2021-EGA-25

University

Semmelweis University

Supervisor

Prof. Zoltán Benyó

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 after complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

6945

Start

14:42

End

14:48