Author, as appears in the article.: Girona J, Rosales R, Saavedra P, Masana L, Vallvé JC
Department: Ciències Mèdiques Bàsiques Medicina i Cirurgia
URV's Author/s: Girona Tell, Josefa / Masana Marín, Luis / ROSALES RIBAS, ROSER / SAAVEDRA GARCIA, PAULA
Keywords: human artery coronary smooth muscle cells inflammation lipid-laden cells migration oxidative stress Activation Adipokines Chain Expression Fatty-acids Glucose Human artery coronary smooth muscle cells Inflammation Lipid-laden cells Migration Nadph oxidase Oleic-acid Oxidative stress Proliferation Protein Receptor
Abstract: Fatty acids are essential to cell functionality and may exert diverging vascular effects including migration, proliferation, oxidative stress, and inflammation. This study examined the effect of palmitate on human coronary artery smooth muscle cell (HCASMC) function. An in vitro wound-healing assay indicated that palmitate decreased HCASMC migration in dose- and time-dependent manners. Furthermore, bromodeoxyuridine incorporation assays indicated that palmitate decreased HCASMC proliferation in a dose-response manner. Palmitate also increased reactive oxygen species formation, malondialdehyde content, and intracellular lipid droplets accompanied with increased fatty acid binding protein 4 expression. Moreover, palmitate induced gene expression (monocyte chemoattractant protein 1, matrix metalloproteinase-2, IL-1?, IL-6, IL-8, and TNF-?) and intracellular protein content (plasminogen activator inhibitor-1 and urokinase plasminogen activator) of inflammatory mediators. Finally, we showed that palmitate activates the transcription factor Nrf2 and the upstream kinases ERK1/2 and Akt in HCASMCs. The inhibitor of Nrf2, trigonelline, significantly attenuated palmitate-induced HCASMC expression of the Nrf2 target gene NQO1. These findings indicate that palmitate might be critically related to HCASMC function by slowing cell migration and proliferation and inducing lipid-laden cells, oxidative stress, and inflammation in part by activation of the Nrf2 transcription factor. Palmitate's activation of proinflammatory Nrf2 signaling may represent a novel mechanism mediating the proatherogenic actions of saturated fatty acids.
Thematic Areas: Astronomia / física Biotecnología Cell biology Ciências agrárias i Ciências biológicas i Ciências biológicas ii Ciências biológicas iii Educação física General medicine Medicina i Medicina ii Medicina iii Medicina veterinaria Physiology
licence for use: https://creativecommons.org/licenses/by/3.0/es/
Author's mail: josefa.girona@urv.cat luis.masana@urv.cat josefa.girona@urv.cat
ISSN: 15221563
Author identifier: 0000-0002-6267-8779 0000-0002-0789-4954 0000-0002-6267-8779
Record's date: 2023-02-26
Papper version: info:eu-repo/semantics/publishedVersion
Link to the original source: https://journals.physiology.org/doi/full/10.1152/ajpcell.00293.2018
Papper original source: American Journal Of Physiology-Cell Physiology. 316 (6): C888-C897
APA: Girona J, Rosales R, Saavedra P, Masana L, Vallvé JC (2019). Palmitate decreases migration and proliferation and increases oxidative stress and inflammation in smooth muscle cells. Role of the Nrf2 signaling pathway.. American Journal Of Physiology-Cell Physiology, 316(6), C888-C897. DOI: 10.1152/ajpcell.00293.2018
Licence document URL: https://repositori.urv.cat/ca/proteccio-de-dades/
Article's DOI: 10.1152/ajpcell.00293.2018
Entity: Universitat Rovira i Virgili
Journal publication year: 2019
Publication Type: Journal Publications