Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Lysophospholipids, Lysophosphatidic Acids and Monoacylglycerols: New Therapeutic Targets in Cardiovascular Diseases?

Thomas Duflot
* ORCID logo ,
Ly Tu
ORCID logo ,
Matthieu Leuillier
,
Hind Messaoudi
,
Déborah Groussard
,
Saïda Azhar
,
Raphaël Thuillet
,
Marc Humbert
,
Vincent Richard
,
Christophe Guignabert
ORCID logo ,
Jérémy Bellien
ORCID logo
Version 1 : Received: 31 August 2021 / Approved: 3 September 2021 / Online: 3 September 2021 (15:19:54 CEST)

A peer-reviewed article of this Preprint also exists.

Duflot, T.; Tu, L.; Leuillier, M.; Messaoudi, H.; Groussard, D.; Feugray, G.; Azhar, S.; Thuillet, R.; Bauer, F.; Humbert, M.; et al. Preventing the Increase in Lysophosphatidic Acids: A New Therapeutic Target in Pulmonary Hypertension? Metabolites, 2021, 11, 784. https://doi.org/10.3390/metabo11110784. Duflot, T.; Tu, L.; Leuillier, M.; Messaoudi, H.; Groussard, D.; Feugray, G.; Azhar, S.; Thuillet, R.; Bauer, F.; Humbert, M.; et al. Preventing the Increase in Lysophosphatidic Acids: A New Therapeutic Target in Pulmonary Hypertension? Metabolites, 2021, 11, 784. https://doi.org/10.3390/metabo11110784.

Abstract

Cardiovascular diseases (CVD) are the leading cause of premature death and disability in humans. Increasing data suggest that CVD is closely related to lipid metabolism and signaling. This study aimed to assess whether circulating lysophospholipids (LPL), lysophosphatidic acids (LPA) and monoacylglycerols (MAG) may be considered as biomarkers of CVD. For this objective, the evolution of the plasma levels of 22 compounds (13 LPL, 6 LPA and 3 MAG) was monitored by liquid chromatography coupled with tandem mass spectrometry (HPLC/MS²) in different rat models of CVD, i.e. angiotensin-II-induced hypertension (HTN), ischemic chronic heart failure (CHF) and sugen/hypoxia(SuHx)-induced pulmonary hypertension (PH). On one hand, there was modest changes on the monitored compounds in HTN (LPA 16:0, 18:1 and 20:4), LPC 16:1) and CHF (LPA 16:0, LPC 18:1 and LPE 16:0 and 18:0) models compared to control rats but these changes were no longer significant after correction for multiple testing. On the other hand, PH was associated with important changes in plasma LPA with a significant increase in the 16:0, 18:1, 18:2, 20:4 and 22:6 species. A deleterious impact of LPA was confirmed on isolated human pulmonary smooth muscle cells with an increase in their proliferation. This study demonstrates that circulating LPA species are increased in rats with PH and may contribute to the pathophysiology of this disease. Additional experiments are needed to assess whether the modulation of LPA signaling in PH may be of interest.

Keywords

lysophospholipids; lysophosphatidic acids; cardiovascular diseases; HPLC-MS/MS; rodent models; pulmonary hypertension; chronic heart failure; hypertension

Subject

Medicine and Pharmacology, Pharmacology and Toxicology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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