Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4

Yang, Ying; Luo, Na; Ren, Ying; Xie, Yong; Chen, Jiayuan; Wang, Xiaoqiao; Gu, Zhen-Jie; Mai, Jing-Ting; Liu, Wenhao; Wu, Maoxiong; Chen, Zhi-Teng; Fang, Yongbiao; Zhang, Haifeng; Zuo, Zhiyi; Wang, Jingfeng; Chen, Yangxin

doi:10.3892/ijmm.2017.3034

Cited by 42 publications

(30 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to the effects observed on neuroinflammation and osteoporosis, a beneficial effect of tocopherols and tocotrienols supplementation has also been documented on the incidence of cardiovascular disease. The formation of macrophage foam cells is a characteristic and an early onset of atherosclerosis (Yang et al, 2017 ). The aortas of cholesterol-administered rabbits have typical atherosclerotic lesions and show increased in CD36 mRNA expression.…”

Section: Role Of Antioxidants In the Prevention Of Age-related Diseasmentioning

confidence: 99%

Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases

et al. 2018

View full text Add to dashboard Cite

Aging is the progressive loss of organ and tissue function over time. Growing older is positively linked to cognitive and biological degeneration such as physical frailty, psychological impairment, and cognitive decline. Oxidative stress is considered as an imbalance between pro- and antioxidant species, which results in molecular and cellular damage. Oxidative stress plays a crucial role in the development of age-related diseases. Emerging research evidence has suggested that antioxidant can control the autoxidation by interrupting the propagation of free radicals or by inhibiting the formation of free radicals and subsequently reduce oxidative stress, improve immune function, and increase healthy longevity. Indeed, oxidation damage is highly dependent on the inherited or acquired defects in enzymes involved in the redox-mediated signaling pathways. Therefore, the role of molecules with antioxidant activity that promote healthy aging and counteract oxidative stress is worth to discuss further. Of particular interest in this article, we highlighted the molecular mechanisms of antioxidants involved in the prevention of age-related diseases. Taken together, a better understanding of the role of antioxidants involved in redox modulation of inflammation would provide a useful approach for potential interventions, and subsequently promoting healthy longevity.

show abstract

Section: Role Of Antioxidants In the Prevention Of Age-related Diseasmentioning

confidence: 99%

Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Whether they could accelerate atherosclerosis formation in vivo remains to be studied. Actually, evidence suggests that it is M1-derived foam cells that could induce endothelial-mesenchymal transition (EndMT) by upregulating CCL4 and increase endothelial permeability and monocyte adhesion which is subsequently followed with plaque formation [60]. Rahman and his colleagues demonstrated that M2 polarization plays an essential role in atherosclerosis regression in a mouse model.…”

Section: M2 Macrophages and Atherosclerosismentioning

confidence: 99%

M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment

Chen

et al. 2019

Neural Plasticity

117

View full text Add to dashboard Cite

Atherosclerosis is a chronic progressive inflammation course, which could induce life-threatening diseases such as stroke and myocardial infarction. Optimal medical treatments for atherosclerotic risk factors with current antihypertensive and lipid-lowering drugs (for example, statins) are widely used in clinical practice. However, many patients with established disease still continue to have recurrent cardiovascular events in spite of treatment with a state-of-the-art therapy. Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality worldwide. Hence, current treatment of atherosclerosis is still far from being satisfactory. Recently, M2 macrophages have been found associated with atherosclerosis regression. The M2 phenotype can secrete anti-inflammatory factors such as IL-10 and TGF-β, promote tissue remodeling and repairing through collagen formation, and clear dying cells and debris by efferocytosis. Therefore, modulators targeting macrophages’ polarization to the M2 phenotype could be another promising treatment strategy for atherosclerosis. Two main signaling pathways, the Akt/mTORC/LXR pathway and the JAK/STAT6 pathway, are found playing important roles in M2 polarization. In addition, researchers have reported several potential approaches to modulate M2 polarization. Inhibiting or activating some kinds of enzymes, affecting transcription factors, or acting on several membrane receptors could regulate the polarization of the M2 phenotype. Besides, biomolecules, for example vitamin D, were found to affect the process of M2 polarization. Pomegranate juice could promote M2 polarization via unclear mechanism. In this review, we will discuss how M2 macrophages affect atherosclerosis regression, signal transduction in M2 polarization, and outline potential targets and compounds that affect M2 polarization, thus controlling the progress of atherosclerosis.

show abstract

“…In order to measure the vascular permeability induced by those cytokines, we have developed a three-dimensional (3D) vascular endothelium in vitro model in which we could manipulate the endothelial barrier function and its permeability [26,32]. Recent lines of evidence have shown that EndMT impairs the barrier function of blood vascular endothelial cells [33]. In order to examine the effects of TGF-β on the permeability of lymphatic vessels, we adapted our in vitro model technology to create a three-dimensional lymphatic endothelium by using HDLECs that were pre-treated with TGF-β2 or SB431542 for 24 h (Fig 3).…”

Section: Tgf-β Alters the Integrity Of Micro-lymphatic Vesselsmentioning

confidence: 99%

TGF-beta and TNF-alpha cooperatively induce mesenchymal transition of lymphatic endothelial cells via activation of Activin signals

et al. 2020

View full text Add to dashboard Cite

Lymphatic systems play important roles in the maintenance of fluid homeostasis and undergo anatomical and physiological changes during inflammation and aging. While lymphatic endothelial cells (LECs) undergo mesenchymal transition in response to transforming growth factor-β (TGF-β), the molecular mechanisms underlying endothelial-to-mesenchymal transition (EndMT) of LECs remain largely unknown. In this study, we examined the effect of TGF-β2 and tumor necrosis factor-α (TNF-α), an inflammatory cytokine, on EndMT using human skin-derived lymphatic endothelial cells (HDLECs). TGF-β2-treated HDLECs showed increased expression of SM22α, a mesenchymal cell marker accompanied by increased cell motility and vascular permeability, suggesting HDLECs to undergo EndMT. Our data also revealed that TNF-α could enhance TGF-β2-induced EndMT of HDLECs. Furthermore, both cytokines induced the production of Activin A while decreasing the expression of its inhibitory molecule Follistatin, and thus enhancing EndMT. Finally, we demonstrated that human dermal lymphatic vessels underwent EndMT during aging, characterized by double immunostaining for LYVE1 and SM22α. These results suggest that both TGF-β and TNF-α signals play a central role in EndMT of LECs and could be potential targets for senile edema.

show abstract

Macrophage-derived foam cells impair endothelial barrier function by inducing endothelial-mesenchymal transition via CCL-4

Cited by 42 publications

References 54 publications

Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases

Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases

M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment

TGF-beta and TNF-alpha cooperatively induce mesenchymal transition of lymphatic endothelial cells via activation of Activin signals

Contact Info

Product

Resources

About