ROS-AKT-mTOR axis mediates autophagy of human umbilical vein endothelial cells induced by cooking oil fumes-derived fine particulate matters in vitro

Ding, Rui; Zhang, Chao; Zhu, Xiaoxia; Cheng, Han; Zhu, Furong; Xu, Yachun; Liu, Ying; Wen, Longping; Cao, Jiyu

doi:10.1016/j.freeradbiomed.2017.10.386

Cited by 61 publications

(34 citation statements)

References 25 publications

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“…45 It is generally accepted that ROS are tumour suppressors that are implicated in tumorigenesis, progression and survival phenotypes. 47,48 ROS is a double-edged sword and the influence of ROS within cancer cells, whether they are favourable or harmful, may depend on several factors, such as cell type, stimulus, duration, specificity and levels of ROS. 47,48 ROS is a double-edged sword and the influence of ROS within cancer cells, whether they are favourable or harmful, may depend on several factors, such as cell type, stimulus, duration, specificity and levels of ROS.…”

Section: Discussionmentioning

confidence: 99%

Targeting the ROS/PI3K/AKT/HIF‐1α/HK2 axis of breast cancer cells: Combined administration of Polydatin and 2‐Deoxy‐d‐glucose

Zhang

Zhu

et al. 2019

J Cellular Molecular Medi

109

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It is well established that cancer cells depend upon aerobic glycolysis to provide the energy they need to survive and proliferate. However, anti‐glycolytic agents have yielded few positive results in human patients, in part due to dose‐limiting side effects. Here, we discovered the unexpected anti‐cancer efficacy of Polydatin (PD) combined with 2‐deoxy‐D‐glucose (2‐DG), which is a compound that inhibits glycolysis. We demonstrated in two breast cell lines (MCF‐7 and 4T1) that combination treatment with PD and 2‐DG induced cell apoptosis and inhibited cell proliferation, migration and invasion. Furthermore, we determined the mechanism of PD in synergy with 2‐DG, which decreased the intracellular reactive oxygen (ROS) levels and suppressed the PI3K/AKT pathway. In addition, the combined treatment inhibited the glycolytic phenotype through reducing the expression of HK2. HK2 deletion in breast cancer cells thus improved the anti‐cancer activity of 2‐DG. The combination treatment also resulted in significant tumour regression in the absence of significant morphologic changes in the heart, liver or kidney in vivo. In summary, our study demonstrates that PD synergised with 2‐DG to enhance its anti‐cancer efficacy by inhibiting the ROS/PI3K/AKT/HIF‐1α/HK2 signalling axis, providing a potential anti‐cancer strategy.

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Section: Discussionmentioning

confidence: 99%

Targeting the ROS/PI3K/AKT/HIF‐1α/HK2 axis of breast cancer cells: Combined administration of Polydatin and 2‐Deoxy‐d‐glucose

Zhang

Zhu

et al. 2019

J Cellular Molecular Medi

109

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“…Autophagy is widely involved in physiological and pathological activities of endothelial cells. 11 It is worth noting that it can be induced by mechanical and biochemical factors, including shear stress, calcium and oxidative stress, [15][16][17] which are also influenced by decompression-induced intravascular bubbles. [18][19][20][21][22] We speculated that autophagy was probably involved in bubble-induced endothelial injury.…”

Section: Discussionmentioning

confidence: 99%

“…No. S2767) and was directly dissolved into the culture medium at the concentrations of 5 mmol/L for 24 hours to inhibit autophagy …”

Section: Methodsmentioning

confidence: 99%

“…The role of autophagy involved in endothelial injury in atherosclerosis, ischaemia‐reperfusion, hepatopulmonary syndrome and other diseases has been well studied . It can be induced by both physical and chemical stimuli, including shear stress, calcium and oxidative stress . Intravascular bubbles can disrupt blood flow or even occlude vessels, resulting in altered shear stress and ischaemia‐reperfusion injury .…”

Section: Introductionmentioning

confidence: 99%

“…[12][13][14] It can be induced by both physical and chemical stimuli, including shear stress, calcium and oxidative stress. [15][16][17] Intravascular bubbles can disrupt blood flow or even occlude vessels, resulting in altered shear stress and ischaemiareperfusion injury. 18,19 Bubbles have also been reported to induce increased intracellular calcium in human umbilical vein endothelial cells (HUVECs).…”

mentioning

confidence: 99%

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Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

Wang¹,

Zhang²,

Nie³

et al. 2019

J Cellular Molecular Medi

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Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble‐induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3‐methyladenine (3‐MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3‐II/I ratio and Beclin‐1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase‐3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3‐II/I ratio and partially reversed by 3‐MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre‐conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre‐conditioning, and 30‐minutes pre‐conditioning induced opposing changes, all of which were inhibited by 3‐MA. In conclusion, autophagy was involved and played a biphasic role in bubble‐induced endothelial injury.

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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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ROS-AKT-mTOR axis mediates autophagy of human umbilical vein endothelial cells induced by cooking oil fumes-derived fine particulate matters in vitro

Cited by 61 publications

References 25 publications

Targeting the ROS/PI3K/AKT/HIF‐1α/HK2 axis of breast cancer cells: Combined administration of Polydatin and 2‐Deoxy‐d‐glucose

Targeting the ROS/PI3K/AKT/HIF‐1α/HK2 axis of breast cancer cells: Combined administration of Polydatin and 2‐Deoxy‐d‐glucose

Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

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

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