» Articles » PMID: 34375151

Effects of Fatty Acid Nitroalkanes on Signal Transduction Pathways and Airway Macrophage Activation

Overview
Journal Innate Immun
Publisher Sage Publications
Date 2021 Aug 10
PMID 34375151
Authors
Affiliations
Soon will be listed here.
Abstract

Fatty acid nitroalkenes are reversibly-reactive electrophiles that are endogenously detectable at nM concentrations and display anti-inflammatory, pro-survival actions. These actions are elicited through the alteration of signal transduction proteins via a Michael addition on nucleophilic cysteine thiols. Nitrated fatty acids (NO-FAs), like 9- or 10-nitro-octadec-9-enolic acid, will act on signal transduction proteins directly or on key regulatory proteins to cause an up-regulation or down-regulation of the protein's expression, yielding an anti-inflammatory response. These responses have been characterized in many organ systems, such as the cardiovascular system, with the pulmonary system less well defined. Macrophages are one of the most abundant immune cells in the lung and are essential in maintaining lung homeostasis. Despite this, macrophages can play a role in both acute and chronic lung injury due to up-regulation of anti-inflammatory signal transduction pathways and down-regulation of pro-inflammatory pathways. Through their propensity to alter signal transduction pathways, NO-FAs may be able to reduce macrophage activation during pulmonary injury. This review will focus on the implications of NO-FAs on macrophage activation in the lung and the signal transduction pathways that may be altered, leading to reduced pulmonary injury.

References
1.
Mollenhauer M, Mehrkens D, Rudolph V . Nitrated fatty acids in cardiovascular diseases. Nitric Oxide. 2018; . DOI: 10.1016/j.niox.2018.03.016. View

2.
Diaz-Amarilla P, Miquel E, Trostchansky A, Trias E, Ferreira A, Freeman B . Electrophilic nitro-fatty acids prevent astrocyte-mediated toxicity to motor neurons in a cell model of familial amyotrophic lateral sclerosis via nuclear factor erythroid 2-related factor activation. Free Radic Biol Med. 2016; 95:112-20. PMC: 4867302. DOI: 10.1016/j.freeradbiomed.2016.03.013. View

3.
Louis C, Burns C, Wicks I . TANK-Binding Kinase 1-Dependent Responses in Health and Autoimmunity. Front Immunol. 2018; 9:434. PMC: 5845716. DOI: 10.3389/fimmu.2018.00434. View

4.
Zhang D, Hannink M . Distinct cysteine residues in Keap1 are required for Keap1-dependent ubiquitination of Nrf2 and for stabilization of Nrf2 by chemopreventive agents and oxidative stress. Mol Cell Biol. 2003; 23(22):8137-51. PMC: 262403. DOI: 10.1128/MCB.23.22.8137-8151.2003. View

5.
Yeh C, Shih H, Hong H, Lee S, Yang M, Chen C . Protective effect of wogonin on proinflammatory cytokine generation via Jak1/3-STAT1/3 pathway in lipopolysaccharide stimulated BV2 microglial cells. Toxicol Ind Health. 2013; 31(10):960-6. DOI: 10.1177/0748233713485886. View