Automobile diesel exhaust particles induce lipid droplet formation in macrophages in vitro

Objectives: Diesel exhaust particles (DEP)s are notorious ambient pollutants composed of a complex mixture of a carbon core and diverse chemical irritants. Several studies have demonstrated significant relationships between DEP exposure and serious nasal inflammatory response in vitro, but available information regarding underlying networks in terms of gene expression changes has not sufficiently explained potential mechanisms of DEP-induced nasal damage, especially in vivo. Methods: In the present study, we identified DEP-induced gene expression profiles under short-term and long-term exposure, and identified signaling pathways based on microarray data for understanding effects of DEP exposure in the mouse nasal cavity. Results: Alteration in gene expression due to DEP exposure provokes an imbalance of the immune system via dysregulated inflammatory markers, predicted to disrupt protective responses against harmful exogenous substances in the body. Several candidate markers were identified after validation using qRT-PCR, including S100A9, CAMP, IL20, and S100A8. Conclusions: Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our in vivo results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.

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Aggregation and fusion of low-density lipoproteins in vivo and in vitro

BioMolecular Concepts ◽

10.1515/bmc-2013-0016 ◽

2013 ◽

Vol 4 (5) ◽

pp. 501-518 ◽

Cited By ~ 30

Author(s):

Mengxiao Lu ◽

Olga Gursky

Keyword(s):

Lipid Droplet ◽

Current Knowledge ◽

Single Copy ◽

Droplet Formation ◽

Low Density Lipoproteins ◽

Low Density ◽

Atherosclerotic Lesions ◽

Lipid Droplet Formation

AbstractLow-density lipoproteins (LDLs, also known as ‘bad cholesterol’) are the major carriers of circulating cholesterol and the main causative risk factor of atherosclerosis. Plasma LDLs are 20- to 25-nm nanoparticles containing a core of cholesterol esters surrounded by a phospholipid monolayer and a single copy of apolipoprotein B (550 kDa). An early sign of atherosclerosis is the accumulation of LDL-derived lipid droplets in the arterial wall. According to the widely accepted ‘response-to-retention hypothesis’, LDL binding to the extracellular matrix proteoglycans in the arterial intima induces hydrolytic and oxidative modifications that promote LDL aggregation and fusion. This enhances LDL uptake by the arterial macrophages and triggers a cascade of pathogenic responses that culminate in the development of atherosclerotic lesions. Hence, LDL aggregation, fusion, and lipid droplet formation are important early steps in atherogenesis. In vitro, a variety of enzymatic and nonenzymatic modifications of LDL can induce these reactions and thereby provide useful models for their detailed analysis. Here, we summarize current knowledge of the in vivo and in vitro modifications of LDLs leading to their aggregation, fusion, and lipid droplet formation; outline the techniques used to study these reactions; and propose a molecular mechanism that underlies these pro-atherogenic processes. Such knowledge is essential in identifying endogenous and exogenous factors that can promote or prevent LDL aggregation and fusion in vivo and to help establish new potential therapeutic targets to decelerate or even block these pathogenic reactions.

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Mechanism of Apparent Inhibition of Superoxide Dismutase Activity In Vitro by Diesel Exhaust Particles (Proceedings of the 20th Symposium on Toxicology and Environmental Health)

Eisei kagaku ◽

10.1248/jhs1956.41.p8 ◽

1995 ◽

Vol 41 (1) ◽

pp. P8-P8

Author(s):

YOSHITO KUMAGAI ◽

JUNSEI TAIRA ◽

MASARU SAGAI

Keyword(s):

Superoxide Dismutase ◽

Environmental Health ◽

Diesel Exhaust ◽

Diesel Exhaust Particles ◽

Superoxide Dismutase Activity ◽

Exhaust Particles

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Comparison of inflammatory cytokine release from nasal epithelial cells of non-atopic non-rhinitic, allergic rhinitic and polyp subjects and effects of diesel exhaust particles in vitro

Allergologia et Immunopathologia ◽

10.1016/j.aller.2016.10.015 ◽

2017 ◽

Vol 45 (5) ◽

pp. 473-481 ◽

Cited By ~ 11

Author(s):

A.B. Ozturk ◽

R. Bayraktar ◽

B. Gogebakan ◽

S. Mumbuc ◽

H. Bayram

Keyword(s):

Epithelial Cells ◽

Diesel Exhaust ◽

Inflammatory Cytokine ◽

Diesel Exhaust Particles ◽

Cytokine Release ◽

Nasal Epithelial Cells ◽

Exhaust Particles

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Effects of diesel exhaust particles on human lung epithelial cells: An in vitro study

Respiratory Medicine ◽

10.1016/j.rmed.2006.11.011 ◽

2007 ◽

Vol 101 (6) ◽

pp. 1155-1162 ◽

Cited By ~ 75

Author(s):

G. Mazzarella ◽

F. Ferraraccio ◽

M.V. Prati ◽

S. Annunziata ◽

A. Bianco ◽

...

Keyword(s):

Epithelial Cells ◽

Diesel Exhaust ◽

Human Lung ◽

In Vitro Study ◽

Diesel Exhaust Particles ◽

Lung Epithelial Cells ◽

Lung Epithelial ◽

Exhaust Particles ◽

Human Lung Epithelial Cells

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Thiazolidinedione-induced lipid droplet formation during osteogenic differentiation

Journal of Endocrinology ◽

10.1530/joe-14-0425 ◽

2014 ◽

Vol 223 (2) ◽

pp. 119-132 ◽

Cited By ~ 9

Author(s):

M van de Vyver ◽

E Andrag ◽

I L Cockburn ◽

W F Ferris

Keyword(s):

Adipose Tissue ◽

Lipid Droplet ◽

Lipid Accumulation ◽

Adipogenic Differentiation ◽

Chronic Administration ◽

Droplet Formation ◽

Pcr Analysis ◽

Mineral Density ◽

Lipid Droplet Formation

Chronic administration of the insulin-sensitising drugs, thiazolidinediones (TZDs), results in low bone mineral density and ‘fatty bones’. This is thought to be due, at least in part, to aberrant differentiation of progenitor mesenchymal stem cells (MSCs) away from osteogenesis towards adipogenesis. This study directly compared the effects of rosiglitazone, pioglitazone, and netoglitazone treatment on osteogenesis and adipogenesis in MSCs derived from subcutaneous (SC) or visceral (PV) white adipose tissue. MSCs were isolated from adipose tissue depots of male Wistar rats and characterised using flow cytometry. The effects of TZD treatment on osteogenic and adipogenic differentiation were assessed histologically (day 14) and by quantitative PCR analysis (Pparγ2(Pparg2),Ap2(Fabp4), Adipsin(Adps),Msx2, Collagen I(Col1a1), andAlp) on days 0, 7, and 10. Uniquely, lipid droplet formation and mineralisation were found to occur concurrently in response to TZD treatment during osteogenesis. Compared with SC MSCs, PV MSCs were more prone to lipid accumulation under controlled osteogenic and adipogenic differentiation conditions. This study demonstrated that the extent of lipid accumulation is dependent on the nature of thePparligand and that SC and PV MSCs respond differently toin vitroTZD treatment, suggesting that metabolic status can contribute to the adverse effects associated with TZD treatment.

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