D-4F, an apoA-1 mimetic, decreases airway hyperresponsiveness, inflammation, and oxidative stress in a murine model of asthma

Nandedkar, S.D.; Weihrauch, Dorothée; Xu, Hao; Shi, Yang; Feroah, Thom R.; Hutchins, William; Rickaby, D. A.; Düzgüneş, Nejat; Hillery, Cheryl A.; Konduri, K.S.; Pritchard, Kirkwood A.

doi:10.1194/jlr.m012724

Cited by 69 publications

(65 citation statements)

References 57 publications

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“…[151][152][153] In the context of lung disease, 4F decreases airway hyperresponsiveness, inflammation, and oxidative stress in a murine model of asthma. 154 We have recently demonstrated that the levels of oxidized lipids are elevated in the plasma of PH rats, 56 as well as in PAH patients, 29 and may contribute to the inflammatory response and vascular changes involved in the progression of PH. Therapy with 4F has been shown to be very effective in restoring the levels of oxidized lipids and rescue of preexisting PH in animal models.…”

Section: Novel Therapeutic Strategies In Pahmentioning

confidence: 99%

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

et al. 2016

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Pulmonary arterial hypertension (PAH) is a multifactorial disease characterized by interplay of many cellular, molecular, and genetic events that lead to excessive proliferation of pulmonary cells, including smooth muscle and endothelial cells; inflammation; and extracellular matrix remodeling. Abnormal vascular changes and structural remodeling associated with PAH culminate in vasoconstriction and obstruction of pulmonary arteries, contributing to increased pulmonary vascular resistance, pulmonary hypertension, and right ventricular failure. The complex molecular mechanisms involved in the pathobiology of PAH are the limiting factors in the development of potential therapeutic interventions for PAH. Over the years, our group and others have demonstrated the critical implication of lipids in the pathogenesis of PAH. This review specifically focuses on the current understanding of the role of oxidized lipids, lipid metabolism, peroxidation, and oxidative stress in the progression of PAH. This review also discusses the relevance of apolipoprotein A-I mimetic peptides and microRNA-193, which are known to regulate the levels of oxidized lipids, as potential therapeutics in PAH.

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Section: Novel Therapeutic Strategies In Pahmentioning

confidence: 99%

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

et al. 2016

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“…For example, apoA-I mimetic peptides prevented increases in neutrophilic airway inflammation in OVA-challenged Apoa1-deficient mice (57). Similarly, administration of apoA-I mimetic peptides or human apoA-I to murine models of experimental allergic asthma suppressed airway inflammation with decreases in BALF inflammatory cells (e.g., eosinophils, neutrophils, and lymphocytes), type 2 and type 17 cytokines, airway epithelial cytokines (IL-25, IL-33, thymic stromal lymphopoietin), C-C chemokines, and alternative macrophage activation, and increased lipoxin A4 (63,71,72). In addition, apoA-I mimetic peptides or human apoA-I attenuated increases in AHR, MCM, transforming growth factor (TGF)-b, and lung collagen deposition, and improved airway epithelial cell barrier function.…”

Section: Apoa-i and Asthmamentioning

confidence: 99%

Emerging Roles of Apolipoprotein E and Apolipoprotein A-I in the Pathogenesis and Treatment of Lung Disease

Yao

Gordon

Figueroa

et al. 2016

Am J Respir Cell Mol Biol

116

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“…Understanding the mechanisms regulating the interaction of apoA-I with ABCA1 would clarify the molecular details of cellular cholesterol efflux and further help to develop strategies to increase plasma HDL concentrations. In addition to lipid metabolism regulation, apoA-I/ABCA1 interaction is involved in the process of apoptosis and inflammation, which also were thought to play crucial roles in the development of atherosclerosis (12)(13)(14). Therefore, the interaction of apoA-I with ABCA1 could connect inflammation and RCT in vivo.…”

Section: Introductionmentioning

confidence: 99%

The Interaction of ApoA-I and ABCA1 Triggers Signal Transduction Pathways to Mediate Efflux of Cellular Lipids

Zhao

Yin

et al. 2011

Mol Med

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Reverse cholesterol transport (RCT) has been characterized as a crucial step for antiatherosclerosis, which is initiated by ATPbinding cassette A1 (ABCA1) to mediate the efflux of cellular phospholipids and cholesterol to lipid-free apolipoprotein A-I (apoA-I). However, the mechanisms underlying apoA-I/ABCA1 interaction to lead to the lipidation of apoA-I are poorly understood. There are several models proposed for the interaction of apoA-I with ABCA1 as well as the lipidation of apoA-I mediated by ABCA1. ApoA-I increases the levels of ABCA1 protein markedly. In turn, ABCA1 can stabilize apoA-I. The interaction of apoA-I with ABCA1 could activate signaling molecules that modulate posttranslational ABCA1 activity or lipid transport activity. The key signaling molecules in these processes include protein kinase A (PKA), protein kinase C (PKC), Janus kinase 2 (JAK2), Rho GTPases and Ca 2+ , and many factors also could influence the interaction of apoA-I with ABCA1. This review will summarize these mechanisms for the apoA-I interaction with ABCA1 as well as the signal transduction pathways involved in these processes.

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D-4F, an apoA-1 mimetic, decreases airway hyperresponsiveness, inflammation, and oxidative stress in a murine model of asthma

Cited by 69 publications

References 57 publications

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

Role of Oxidized Lipids in Pulmonary Arterial Hypertension

Emerging Roles of Apolipoprotein E and Apolipoprotein A-I in the Pathogenesis and Treatment of Lung Disease

The Interaction of ApoA-I and ABCA1 Triggers Signal Transduction Pathways to Mediate Efflux of Cellular Lipids

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