Expression of cytokine genes in the aorta is altered by the deficiency in MCP-1: Effect of a high-fat, high-cholesterol diet

Rull, Anna; Beltrán‐Debón, Raúl; Aragonès, Gerard; Rodríguez-Sanabria, Fernando; Alonso-Villaverde, Carlos; Camps, Jordi; Joven, Jorge

doi:10.1016/j.cyto.2010.02.010

Cited by 20 publications

(18 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, all these actions may vary under different experimental conditions and appear to differ between normal and hyperlipidaemic models. The interpretation of data in these models is even more difficult because the expression of other chemokine genes in tissues is highly influenced by both the absence of CCL2 and dietary fat and cholesterol (Rull et al 2010a). It is of note that lipid peroxidation, particularly that of lysophosphatidylcholine, and the consequent oxidative stress and oversecretion of CCL2 have been recently implicated in early stages of adipose tissue inflammation through a mechanism that involves MEK/ ERK, tyrosine kinase, and (to a lesser extent) protein kinase C (PKC) (Rong et al 2002;Steinbrecher et al 1984).…”

Section: Discussionmentioning

confidence: 99%

“…There are no systematic data on tissue distribution but wide distribution is also suspected. Moreover, the chemokine system is highly redundant such that a deficiency in one does not blunt the inflammatory response (Rull et al 2010a). Chemokines are involved in attracting monocytes to sites of inflammation in a number of diseases including atherosclerosis, pulmonary fibrosis and both degenerative and inflammatory arthritis (Rull et al 2010b).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tissue distribution and expression of paraoxonases and chemokines in mouse: the ubiquitous and joint localisation suggest a systemic and coordinated role

et al. 2010

Self Cite

View full text Add to dashboard Cite

A vicious cycle between oxidation and inflammation leads to complications in a growing number of disease states. Knowledge on tissue distribution of chemokines, mediators of inflammatory response, and paraoxonases, with antioxidant and anti-inflammatory actions, may be relevant. Using immunohistochemistry and quantitative real-time PCR we have investigated the distribution of PON1, 2 and 3, CCL2, 7, 8 and 12 and the chemokine receptor CCR2 protein and mRNA in 23 tissues from C57BL/6J mice. As expected, PON1, 2 and 3, CCL2, 7, 8 and 12 and CCR2 proteins were present in the vast majority of tissues investigated. Surprisingly, mRNA for these proteins was also expressed in most of these tissues suggesting local production and the ability to respond in situ to inflammatory stimuli. The wide distribution and expression of mRNA for paraoxonases and CC-chemokines suggest a systemic, probably coordinated, role in the overall inflammatory response.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tissue distribution and expression of paraoxonases and chemokines in mouse: the ubiquitous and joint localisation suggest a systemic and coordinated role

et al. 2010

Self Cite

View full text Add to dashboard Cite

show abstract

“…LPC stimulates the cellular production of MCP-1 at the transcription level through a mechanism that involves MEK/ERK, tyrosine kinase, and (to a lesser extent) protein kinase C (PKC) [85]. More recent data suggest that 12/15-lipoxygenase (12/15LO) is required for early onset high-fat-diet-induced adipose tissue inflammation and insulin resistance in mice [86]. Cells overexpressing 12/15LO secrete an excess of MCP-1 and, correspondingly, adipose tissues from 12/15LO knockout (KO) mice fed a high-fat diet are not infiltrated by macrophages, do not show any increase in inflammatory markers, and do not exhibit changes in insulin-stimulated glucose disposal rate or of hepatic glucose output.…”

Section: Combined Functioning Of Pon1 and Mcp-1 In Regulating Inflmentioning

confidence: 99%

PPARs in Regulation of Paraoxonases: Control of Oxidative Stress and Inflammation Pathways

et al. 2012

Self Cite

View full text Add to dashboard Cite

The paraoxonase (PON) group of enzymes, composed of PON1, PON2, and PON3, play an important role in decreasing oxidative stress by degrading lipid peroxides. PON1 synthesis is upregulated by PPAR. Several pharmacological compounds (acting as antioxidants and, hence, atheroprotective) stimulate both PPAR activity and PON1 expression. Recent evidence suggests that PON1 and the monocyte chemoattractant protein-1 (MCP-1) are involved in coordinating the inflammatory response in damaged tissues; PPAR may be central in the regulation of these biochemical pathways. This article reviews the state of knowledge on PON1 biochemistry and function, the influence of genetic variation, and the regulation of PON1 expression by pharmaceutical compounds that increase PPAR activity. We also describe recent lines of evidence suggesting links between PON1 and MCP-1 and how their production may be regulated by PPAR.

show abstract

“…And the failure of some hormones with structurally the same signaling pathway as cytokines to secrete can reduce insulin sensitivity, which may lead to the development of type 2 diabetes, cardiovascular diseases, and atherosclerosis [2]. …”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have shown that the expression of MCP-1 is much more marked in mice fed a high fat diet, and similarly associated chemokines interact with each other [2]. The expression of MCP-1 is affected by the production of reactive oxygen species, which include signaling molecules such as ERK (extra cellular signal regulate kinase), Mn-SOD (manganese containing superoxide dismutase), HIF-1 (hypoxia inducible factor), and NOX (nitric oxide synthase).…”

Section: Introductionmentioning

confidence: 99%

Combined influence of dietary restriction and treadmill running on MCP-1 and the expression of oxidative stress-related mRNA in the adipose tissue in obese mice

Ahn¹,

Kim²

2014

Journal of Exercise Nutrition and Biochemistry

View full text Add to dashboard Cite

[Purpose]This study suggests that the negative effects of inflammation caused by obesity could be prevented through diet restriction and exercise.[Methods]In this study, 44 C57/BL6 male mice at about 4 weeks old (Orient bio, South Korea) were given a high fat diet for 5 weeks to make them obese. To help the mice lose weight, their dietary intake was limited and they were exercised on the treadmill for 8 weeks, and during that period, we analyzed the changes of MCP-1, ERK, Mn-SOD, HIF-1, and NOX in epididymal adipose tissue. There ND control group and obese group with high fat diet (HFD), and it is divided into four groups; HFD-ND-EX group, HFD-ND-nonEX group, HFD-DR-EX group and HFD-DR-nonEX group.[Results]During their progress, the mRNA expressions of HIF-1α and ERK2 decreased, as did the expression of MCP-1 contained in the nucleus by suppressing oxygen free radicals, which was observed after the exercise program. However, dietary restriction without exercise training triggered an increase in the mRNA expression of MCP-1.[Conclusion]To put this in perspective, combining exercise and dietary intake restriction likely prevented an influx of macrophages by reducing the number of fat cells, whereas only dietary restriction was not effective against reducing inflammation.

show abstract

Expression of cytokine genes in the aorta is altered by the deficiency in MCP-1: Effect of a high-fat, high-cholesterol diet

Cited by 20 publications

References 44 publications

Tissue distribution and expression of paraoxonases and chemokines in mouse: the ubiquitous and joint localisation suggest a systemic and coordinated role

Tissue distribution and expression of paraoxonases and chemokines in mouse: the ubiquitous and joint localisation suggest a systemic and coordinated role

PPARs in Regulation of Paraoxonases: Control of Oxidative Stress and Inflammation Pathways

Combined influence of dietary restriction and treadmill running on MCP-1 and the expression of oxidative stress-related mRNA in the adipose tissue in obese mice

Contact Info

Product

Resources

About