Pro-fibrotic effect of oxidized LDL in cardiac myofibroblasts

Monica Villa, Paulina Cerda-Opazo, Danica Jimenez-Gallegos, Valeria Garrido-Moreno, Mario Chiong, Andrew FG Quest, Jorge Toledo, Lorena Garcia

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

Inflammatory signals associated with cardiac diseases trigger trans-differentiation of cardiac fibroblasts to cardiac myofibroblasts. Cardiac myofibroblasts are the main cell type involved in the development of cardiac fibrosis, a diffuse and disproportionate accumulation of collagen in the myocardium. Although the role of the scavenger like-lectin receptor LOX-1 was previously investigated in cardiac fibroblasts and fibrosis, the involvement of the LOX-1 ligand -oxidized low-density lipoprotein (oxLDL)- on cardiac myofibroblast function still remains unexplored. In the present work, we investigated the effect of oxLDL/LOX-1 on fibrotic markers and cardiac myofibroblast function. Our in vitro results showed that oxLDL increased cardiac myofibroblast proliferation, triggered an increase in the synthesis of collagen type I and fibronectin containing extra domain A, and stimulated collagen type I secretion. oxLDL also decreased cardiac myofibroblast migration, collagen gel contraction and cell area, without modifying α-smooth muscle actin protein levels. These effects were dependent on LOX-1, because LOX-1 knockdown abolished oxLDL effects. Collectively these data showed that oxLDL has important modulatory effects on cardiac myofibroblast function.

Original languageEnglish
Pages (from-to)696-701
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume524
Issue number3
DOIs
Publication statusPublished - Apr 9 2020

Bibliographical note

Publisher Copyright:
© 2020 Elsevier Inc.

Funding

This work was supported by Agencia Nacional de Investigacion y Desarrollo (ANID), Chile : This work was supported by FONDECYT 1140713 (LG), Universidad de Chile ENL022/17 , CONICYT PhD fellowship 21140144 (MV), FONDAP 15130011 (LG, MC, AQ). This work was supported by Agencia Nacional de Investigacion y Desarrollo (ANID), Chile: This work was supported by FONDECYT 1140713 (LG), Universidad de Chile ENL022/17, CONICYT PhD fellowship 21140144 (MV), FONDAP 15130011 (LG, MC, AQ).

FundersFunder number
FONDAP
Comisión Nacional de Investigación Científica y Tecnológica21140144
Fondo Nacional de Desarrollo Científico y Tecnológico1140713
Universidad de ChileENL022/17
Agencia de Innovación y Desarrollo de Andalucía
Fondo de Financiamiento de Centros de Investigación en Áreas Prioritarias15130011
Agencia Nacional de Investigación y Desarrollo

    ASJC Scopus Subject Areas

    • Biophysics
    • Biochemistry
    • Molecular Biology
    • Cell Biology

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