Effects of cooking oil fume derived fine particulate matter on blood vessel formation through the VEGF/VEGFR2/MEK1/2/ERK1/2/mTOR pathway in human umbilical vein endothelial cells

Zhu, Furong; Cheng, Han; Lei, Ruoqian; Shen, Chao; Liu, Jie; Hou, Lijuan; Zhang, Chao; Xu, Yachun; Ding, Rui; Cao, Jiyu

doi:10.1016/j.etap.2019.04.008

Cited by 21 publications

(15 citation statements)

References 28 publications

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“…The viability of cells and number of tubes were significantly decreased under COF‐derived PM2.5 exposure in the HUVECs treated with SU5416, a vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor, in a dose‐dependent manner. Therefore, we further conclude the role of VEGFR2‐mitogen activated protein kinase1/2 (MEK1/2)/extracellular regulated protein kinase1/2 (ERK1/2)/mTOR signaling in the COF‐derived PM2.5 inhibition of angiogenesis (Zhu et al, 2019) (Figure 4).…”

Section: The Effects Of Pm25 On Vec Physiological Functionsmentioning

confidence: 57%

“…A previous study found that promotion of intracellular ROS induced the apoptosis of VECs and PM2.5 decreased cell migration and tube formation in a concentration‐dependent manner in HUVECs, suggesting that PM2.5 impacts angiogenesis, which involves cell migration and tube formation (Chen, Wu, et al, 2017). Furthermore, Zhu et al investigated the cytotoxicity of COF‐derived PM2.5 in HUVECs and found that the cell viability declined progressively and was proportional to COF‐derived PM2.5 concentration and exposure time (Zhu et al, 2019). The viability of cells and number of tubes were significantly decreased under COF‐derived PM2.5 exposure in the HUVECs treated with SU5416, a vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor, in a dose‐dependent manner.…”

Section: The Effects Of Pm25 On Vec Physiological Functionsmentioning

confidence: 99%

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The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

Xie

You

Zhi

et al. 2021

J of Applied Toxicology

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Several epidemiologic and toxicological studies have widely regarded ambient fine particulate matter (PM2.5), the particles with an aerodynamic diameter less than 2.5 μm, as a strong potential threat to human health. PM2.5 exposure is mainly through the respiratory tract where it can permeate the lung alveoli and enter the blood circulation. After going into the circulation, PM2.5 directly confronts the vascular endothelial cells (VECs). The VECs, which are lined up in the innermost layer of the blood vessels, are essential in the homeostasis of physiological processes. Thus, the damage and dysfunction of VECs is a common cause of various diseases. In this review, we summarize the toxicity of PM2.5 to VECs including the pathophysiological mechanism and the effects of VEC‐mediated physiological functions. The review has discussed the association of impaired VEC function by PM2.5 with various diseases, indicating that the VECs may be an effective assessment of public health recommendations under PM2.5 exposure. Therefore, reducing the adverse effect of PM2.5 on VECs will prevent the potential occurrence and fatality of the relevant diseases in the future.

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Section: The Effects Of Pm25 On Vec Physiological Functionsmentioning

confidence: 57%

Section: The Effects Of Pm25 On Vec Physiological Functionsmentioning

confidence: 99%

The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

Xie

You

Zhi

et al. 2021

J of Applied Toxicology

View full text Add to dashboard Cite

show abstract

“…Owing to the higher tyrosinase activity of VEGFR2 relative to VEGFR1, the VEGF/VEGFR2 signaling pathway is widely considered as the most important regulatory pathway in angiogenesis, which is involved throughout the process. Many studies indicate that this pathway activates the Erk1/2 signaling pathway through the tandem reaction process and induces biological changes in VEC, including proliferation, migration, tube formation, and vascular permeability, in turn, exacerbating angiogenesis in RA (Shibuya, 2015; Yamaguchi, Sudo, & Imai, 2019; Zhu et al, 2019). Our findings suggest that RASFs exert a stimulatory effect on HUVECs by promoting the secretion of proangiogenic factors and disrupting the balance cytokines in the MH7A inflammatory microenvironment.…”

Section: Discussionmentioning

confidence: 99%

Geniposide downregulates the VEGF/SphK1/S1P pathway and alleviates angiogenesis in rheumatoid arthritis in vivo and in vitro

Wang

Hong

Deng

et al. 2021

Phytotherapy Research

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The VEGF/SphK1/S1P pathway is closely related to angiogenesis in rheumatoid arthritis (RA), but the precise underlying mechanisms are unclear at present. Here, we explored the involvement of the VEGF/SphK1/S1P cascade in RA models and determined the effects of GE intervention. Our results showed abnormal expression of proteins related to this pathway in RA synovial tissue. Treatment with GE effectively regulated the signal axis, inhibited angiogenesis, and alleviated RA symptoms. In vitro, TNF‐ɑ enhanced the VEGF/SphK1/S1P pathway in a co‐culture model of fibroblast‐like synoviocytes (FLS) and vascular endothelial cells (VEC). GE induced downregulation of VEGF in FLS, restored the dynamic balance of pro‐/antiangiogenic factors, and suppressed SphK1/S1P signaling in VEC, resulting in lower proliferation activity, migration ability, tube formation ability, and S1P secretion ability of VEC cells. Additionally, SphK1‐specific small interfering RNA (siRNA) blocked the VEGF/SphK1/S1P cascade, which can effectively alleviate the stimulatory effect of FLS on VEC and further enhanced the therapeutic effect of GE. Taken together, our results demonstrate that GE suppresses the VEGF/SphK1/S1P pathway and alleviates the stimulation of VEC by FLS, thereby preventing angiogenesis and promoting therapeutic effects against RA.

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“…Indoor particles impair microvascular function through inflammation and oxidative stress [179]. Cooking oil fumes (COFs), the main pollutants in kitchen air, can significantly reduce cellular viability, and inhibit angiogenesis in HUVECs through the ROS-mediated NLRP3 inflammasome pathway or VEGF/VEGFR2/MEK1/2/ERK1/2/ mTOR pathway [40,119]. COF-derived PM 2.5 mediates autophagy via the ROS/AKT/mTOR axis in HUVECs [180].…”

Section: Indoor Pm 25 Elicits Endothelial Dysfunction and Atherosclementioning

confidence: 99%

The critical role of endothelial function in fine particulate matter-induced atherosclerosis

et al. 2020

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Ambient and indoor air pollution contributes annually to approximately seven million premature deaths. Air pollution is a complex mixture of gaseous and particulate materials. In particular, fine particulate matter (PM2.5) plays a major mortality risk factor particularly on cardiovascular diseases through mechanisms of atherosclerosis, thrombosis and inflammation. A review on the PM2.5-induced atherosclerosis is needed to better understand the involved mechanisms. In this review, we summarized epidemiology and animal studies of PM2.5-induced atherosclerosis. Vascular endothelial injury is a critical early predictor of atherosclerosis. The evidence of mechanisms of PM2.5-induced atherosclerosis supports effects on vascular function. Thus, we summarized the main mechanisms of PM2.5-triggered vascular endothelial injury, which mainly involved three aspects, including vascular endothelial permeability, vasomotor function and vascular reparative capacity. Then we reviewed the relationship between PM2.5-induced endothelial injury and atherosclerosis. PM2.5-induced endothelial injury associated with inflammation, pro-coagulation and lipid deposition. Although the evidence of PM2.5-induced atherosclerosis is undergoing continual refinement, the mechanisms of PM2.5-triggered atherosclerosis are still limited, especially indoor PM2.5. Subsequent efforts of researchers are needed to improve the understanding of PM2.5 and atherosclerosis. Preventing or avoiding PM2.5-induced endothelial damage may greatly reduce the occurrence and development of atherosclerosis.

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Effects of cooking oil fume derived fine particulate matter on blood vessel formation through the VEGF/VEGFR2/MEK1/2/ERK1/2/mTOR pathway in human umbilical vein endothelial cells

Cited by 21 publications

References 28 publications

The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

Geniposide downregulates the VEGF/SphK1/S1P pathway and alleviates angiogenesis in rheumatoid arthritis in vivo and in vitro

The critical role of endothelial function in fine particulate matter-induced atherosclerosis

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