Monocyte chemoattractant protein-1 (MCP-1) and fibroblast growth factor-21 (FGF-21) as biomarkers of subclinical atherosclerosis in women

Basurto, Lourdes; Gregory, Michael; Hernández, Susana Barrera; Sánchez-Huerta, Lucero; Martínez, Alma Díaz; Manuel‐Apolinar, Leticia; Avelar, Francisco; Alonso, Laura Alejandra Mejía; Sánchez-Arenas, Rosalinda

doi:10.1016/j.exger.2019.05.013

Cited by 28 publications

(25 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Under normal circumstances, thrombomodulin blocks the expression of HMGB1, but in atherosclerosis, thrombomodulin is downregulated, thereby allowing unmitigated expression of HMGB1. 27 Previous research has shown that TNF-α-mediated inflammatory response in HAECs involves HMGB1-mediated activation of Tolllike receptor 4. 24 Additionally, HMGB1 triggers further upregulation of TNF-α, thereby initiating a sort of positive feedback loop.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

<p>Laquinimod Protects Against TNF-α-Induced Attachment of Monocytes to Human Aortic Endothelial Cells (HAECs) by Increasing the Expression of KLF2</p>

Jiang

Zhang

Wang

2020

DDDT

View full text Add to dashboard Cite

Introduction: As a worldwide health issue, the treatment and prevention of atherosclerosis present an important goal. Increased levels of proinflammatory cytokines such as TNF-αassociated chronic inflammatory response cause endothelial cells to lose their ability to regulate vascular function. Lipid-laden immune cells are recruited to the endothelium where they adhere to the endothelial wall and invade the intimal space, thereby leading to the development of atherosclerotic lesions, fatty plaques, and thickening of the arterial wall. In the present study, for the first time, we investigated the effects of laquinimod, an immunomodulatory agent used for the treatment of multiple sclerosis, on human aortic endothelial in a TNF-α-induced atherosclerotic microenvironment. At present, the mechanism of action of laquinimod is not well defined. Methods: The effects of laquinimod on the gene expression of IL-6, MCP-1, VCAM-1, E-selectin, and KLF2 were measured by real-time PCR. ELISA assay was used to determine protein secretion and expression. Phosphorylation of ERK5 and the protein level of KLF2 were measured by Western blot analysis. The attachment of monocytes to endothelial cells was assayed by calcein-AM staining and fluorescent microscopy. Results: Our findings demonstrate that laquinimod reduced the expression of key inflammatory cytokines and chemokines, including IL-6, MCP-1, and HMGB1. We further demonstrate that laquinimod significantly reduced the attachment of monocytes to endothelial cells, which is mediated through reduced expression of the cellular adhesion molecules VCAM-1 and E-selectin. Here, we found that laquinimod could significantly increase the expression of KLF2 through activation of ERK5 signaling. The results of our KLF2 knockdown experiment confirm that the effects of laquinimod observed in vitro are dependent on KLF2 expression. Conclusion: Together, these findings suggest a potential antiatherosclerotic capacity of laquinimod. Further research will elucidate the underlying mechanisms.

show abstract

Section: Discussionmentioning

confidence: 99%

“…A recent study found that MCP-1 levels could serve as an early biomarker for atherosclerosis. 27 In a double-blind clinical trial, monocytes extracted from patients treated with laquinimod were found to excrete lower levels of MCP-1. 28 Additionally, research suggests that laquinimod might reduce the expression of MCP-1 in the spinal cord.…”

Section: Discussionmentioning

confidence: 99%

<p>Laquinimod Protects Against TNF-α-Induced Attachment of Monocytes to Human Aortic Endothelial Cells (HAECs) by Increasing the Expression of KLF2</p>

Jiang

Zhang

Wang

2020

DDDT

View full text Add to dashboard Cite

show abstract

“…In EAT from T2DM patients with multivessel CAD, FGF-21 gene expression is reduced [ 317 ], and in patients undergoing cardiac surgery, FGF-21 expression in EAT increases after surgery, suggesting a role protecting from surgery-related inflammatory response [ 319 ]. However, several studies have shown that increased levels of circulating FGF-21 are associated with the presence of atherosclerosis [ 337 , 338 , 339 , 340 , 341 ], although there are contradictory results [ 342 ].…”

Section: Role Of Some Adipokines In Inflammatory Processes Associamentioning

confidence: 99%

Adipokines and Inflammation: Focus on Cardiovascular Diseases

Feijóo‐Bandín

Aragón-Herrera

Moraña-Fernández

et al. 2020

IJMS

View full text Add to dashboard Cite

It is well established that adipose tissue, apart from its energy storage function, acts as an endocrine organ that produces and secretes a number of bioactive substances, including hormones commonly known as adipokines. Obesity is a major risk factor for the development of cardiovascular diseases, mainly due to a low grade of inflammation and the excessive fat accumulation produced in this state. The adipose tissue dysfunction in obesity leads to an aberrant release of adipokines, some of them with direct cardiovascular and inflammatory regulatory functions. Inflammation is a common link between obesity and cardiovascular diseases, so this review will summarise the role of the main adipokines implicated in the regulation of the inflammatory processes occurring under the scenario of cardiovascular diseases.

show abstract

“…Low-grade, systemic inflammation is considered a key contributor in the pathophysiological progression of metabolic disorders including cardiovascular disease (CVD), type 2 diabetes, and metabolic syndrome (1)(2)(3). Indeed, circulating concentrations of C-reactive protein (CRP), cytokines including interleukin (IL)-6, tumor necrosis factor (TNF)-a, their receptors, and monocyte chemoattractant protein (MCP)-1, and cell adhesion molecules including intracellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, have been positively associated with CVD risk (4)(5)(6)(7)(8)(9)(10)(11). In contrast, some cytokines have anti-inflammatory and anti-atherogenic properties, such as adiponectin and IL-10 (12).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Dairy Product and Dairy Protein Intake on Inflammation: A Systematic Review of the Literature

Nieman

Anderson

Cifelli

2020

Journal of the American College of Nutrition

View full text Add to dashboard Cite

Systemic inflammation is associated with obesity and chronic disease risk. Intake of dairy foods is associated with reduced risk of type 2 diabetes and cardiovascular disease; however, the impact of dairy foods on inflammation is not well-established. The objective of this study was to conduct a systematic review to evaluate the effect of dairy product (milk, cheese, and yogurt) and dairy protein consumption on low-grade systemic inflammation in adults without severe inflammatory disorders. A literature search was completed in September 2019 using PubMed and CENTRAL as well as inspection of reference lists from relevant review articles. The search resulted in the identification of 27 randomized controlled trials which were included in this analysis. In the 19 trials which evaluated dairy products, 10 reported no effect of the intervention, while 8 reported a reduction in at least one biomarker of inflammation. All 8 trials that investigated dairy protein intake on markers of inflammation reported no effect of the intervention. The available literature suggests that dairy products and dairy proteins have neutral to beneficial effects on biomarkers of inflammation. Additional clinical studies designed using inflammatory biomarkers as the primary outcome are needed to fully elucidate the effects of dairy intake on inflammation.

show abstract

Monocyte chemoattractant protein-1 (MCP-1) and fibroblast growth factor-21 (FGF-21) as biomarkers of subclinical atherosclerosis in women

Cited by 28 publications

References 39 publications

<p>Laquinimod Protects Against TNF-α-Induced Attachment of Monocytes to Human Aortic Endothelial Cells (HAECs) by Increasing the Expression of KLF2</p>

<p>Laquinimod Protects Against TNF-α-Induced Attachment of Monocytes to Human Aortic Endothelial Cells (HAECs) by Increasing the Expression of KLF2</p>

Adipokines and Inflammation: Focus on Cardiovascular Diseases

The Effects of Dairy Product and Dairy Protein Intake on Inflammation: A Systematic Review of the Literature

Contact Info

Product

Resources

About