Lipid Rafts and <i>Fas</i>/<i>FasL</i> Pathway May Involve in Elaidic Acid-Induced Apoptosis of Human Umbilical Vein Endothelial Cells

Rao, Huan; Ma, Lixin; Xu, Tingting; Li, Jing; Deng, Zeyuan; Fan, Yanting; Li, Hongyan

doi:10.1021/jf404834e

Cited by 10 publications

(15 citation statements)

References 34 publications

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“…Lipid rafts represent a special localization of epidermal growth factor receptors (EGFRs), altering its signaling pathways (10) and transactivation (11). Rao et al have reported that EA can affect Fas/FasL-induced apoptosis via lipid rafts (12). Lipid rafts may play an important role in EGFR signaling in EA-treated cells.…”

Section: Introductionmentioning

confidence: 99%

Pro‑metastatic signaling of the trans fatty acid elaidic acid is associated with lipid rafts

et al. 2018

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Abstract. Trans fatty acids (TFAs) are risk factors for cardiovascular disorders, and the cancer-promoting effects of TFAs have been previously reported. The present study examined the effects and signaling of elaidic acid (EA), a TFA, in colorectal cancer (CRC) cells. Oral intake of EA was found to increase metastasis of HT29 human CRC cells. Results indicated that, in the plasma membrane, EA was integrated into cholesterol rafts, which contain epidermal growth factor receptors (EGFR). EA increased nanog and c-myc, and decreased PGC-1A through lipid raft-associated EGFR signaling in HT29 cells. Depletion of cholesterol by methyl-β-cyclodextrin treatment abrogated the EA-induced stemness and oxidative phosphorylation. Simvastatin treatment also abrogated EA-enhanced tumor growth. These results indicate that EA enhances the stemness by activating EGFR in lipid rafts.

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Section: Introductionmentioning

confidence: 99%

Pro‑metastatic signaling of the trans fatty acid elaidic acid is associated with lipid rafts

et al. 2018

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“…In our previous study, we found that 9 t 18:1 altered the structure of lipid rafts in human umbilical vein endothelial cells (HUVECs) and regulated the expression of receptor proteins in cell membrane. The results strongly suggested the involvement of lipid rafts and Fas receptor in 9 t 18:1‐induced apoptosis and cell cycle . However, whether different classes of TFAs have similar roles is unclear.…”

Section: Introductionmentioning

confidence: 85%

“…HUVECs were provided by College of Medical Sciences, Nanchang University and cultured in DMEM medium containing 10% FBS, 1% penicillin and 1% streptomyocin at 37°C in a 5% CO 2 humidified atmosphere. The lipid raft distraction model was successfully established using our previous method . The cells were divided into six groups: control group (treated with 0.1 M PBS), elaidic acid group (treated with 50 μM 9 t 18:1 for 24 h), linolelaidic acid group (treated with 50 μM 9 t 12 t 18:2 for 24 h), MβCD group (treated with 10 mM MβCD for 50 min), MβCD + 9 t 18:1 group (incubated with 50 μM 9 t 18:1 for 24 h after treatment with 10 mM MβCD for 50 min) and MβCD + 9 t 12 t 18:2 group (incubated with 50 μM 9 t 12 t 18:2 for 24 h after treatment with 10 mM MβCD for 50 min).…”

Section: Methodsmentioning

confidence: 99%

Linolelaidic acid induces apoptosis, cell cycle arrest and inflammation stronger than elaidic acid in human umbilical vein endothelial cells through lipid rafts

Rao

Qiu

et al. 2016

Euro J Lipid Sci & Tech

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Lipid rafts were reported to play important roles in elaidic acid‐induced apoptosis in human umbilical vein endothelial cells (HUVECs). Linolelaidic acid induced cell injury more seriously than elaidic acid. However, whether lipid rafts may play the same roles for linolelaidic acid‐ and elaidic acid‐induced cell injury was unknown. Therefore, the aim of this study was to compare the effect of lipid rafts on linolelaidic acid‐ and elaidic acid‐induced apoptosis, cell cycle arrest and inflammation in HUVECs. The cell viability was significantly decreased, the number of apoptotic cells and cell population in G1 phase were significantly increased in elaidic acid‐ or linolelaidic acid‐treated cells, compared to methyl‐β‐cyclodextrin + trans‐fatty acids‐treated cells. In addition, the expression levels of pro‐apoptotic proteins (caspase‐3, ‐8, Bax, p53) and inflammation factors (vascular cell adhesion molecule‐1, intercellular adhesion molecule, E‐selectin and nitro oxide) were significantly increased, and anti‐apoptotic protein like Bcl‐2 decreased significantly in linolelaidic acid‐treated cells, which were stronger than those in elaidic acid‐treated cells. In conclusion, linolelaidic acid induces a stronger lesion effect on HUVECs through lipid rafts compared to elaidic acid. Practical applications: Different processing method generated different trans fatty acids, such as industrial hydrogenation produced amount of trans 18:1, deep frying with temperature over 200°C generated both trans 18:1 and trans 18:2. Researches reported that trans fatty acids with different saturation had diverse effect on human health, especially cardiovascular disease. This paper found that 9t12t18:2 induced a stronger lesion effect on HUVECs compared with 9t18:1 through lipid rafts, which indicated that we should pay attention to 9t12t18:2 produced from deep frying, and the deep frying temperature should be dropped to reduce the trans 18:2 level. Moreover, the involvement of lipid rafts in trans fatty acids induced apoptosis, cell cycle arrest and inflammation was demonstrated, which provided a scientific basis for the prevention and treatment of cardiovascular disease. Both linoelaidic acid and elaidic acid induced HUVECs apoptosis and increased expression of pro‐apoptotic proteins. However, supplementation of TFAs to MβCD‐treated cells increased the cell viability and significantly decreased the number of apoptotic cells. Moreover, linolelaidic acid induces a stronger lesion effect on HUVECs by lipid rafts mediation compared to elaidic acid.

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“…Bin et al [47] reported that TFA induced apoptosis of HUVEC by caspase pathway and the mitochondria. Moreover, Rao et al [48] have demonstrated that p53 expression increased after TFA treatment mediated by lipid rafts and Fas/FasL pathway. We concluded that elaidic acid increased p53 and decreased Bcl-2 mRNA expression, which contributed to the apoptosis of HUVEC.…”

Section: Elaidic Acid Induced the Downregulation Of Antioxidative Promentioning

confidence: 99%

Potential Pathways Involved in Elaidic Acid Induced Atherosclerosis in Human Umbilical Vein Endothelial Cells

Liang

et al. 2017

Journal of Chemistry

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Researches have demonstrated that trans-fatty acids are related to the progression of atherosclerosis, but the underlying mechanism is not clear till now. In the presented study, two-dimensional electrophoresis based proteomics was used to discover the role of elaidic acid in atherosclerosis. In human umbilical vein endothelial cells (HUVEC), twenty-two and twenty-three differentially expressed proteins were identified in low (50 mol/L) and high (400 mol/L) concentration elaidic acid simulated groups, respectively, comparing with the control group. The expressions of some selected proteins (PSME 3 , XRCC 5 , GSTP 1 , and GSTO 1 ) were validated by qRT-PCR analysis. Western blotting analysis further confirmed that elaidic acid downregulated the expression of PSME 3 and XRCC 5 . Moreover, P53, the downstream protein of PSME 3 , was further investigated. Results demonstrated that a variety of proteins, many of which were related to oxidative stress, apoptosis, and DNA damage, were involved in the elaidic acid induced atherosclerosis. Furthermore, P53 was demonstrated to regulate the atherosclerosis through cell cycle arrest and apoptosis pathway.

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Lipid Rafts and Fas/FasL Pathway May Involve in Elaidic Acid-Induced Apoptosis of Human Umbilical Vein Endothelial Cells

Cited by 10 publications

References 34 publications

Pro‑metastatic signaling of the trans fatty acid elaidic acid is associated with lipid rafts

Pro‑metastatic signaling of the trans fatty acid elaidic acid is associated with lipid rafts

Linolelaidic acid induces apoptosis, cell cycle arrest and inflammation stronger than elaidic acid in human umbilical vein endothelial cells through lipid rafts

Potential Pathways Involved in Elaidic Acid Induced Atherosclerosis in Human Umbilical Vein Endothelial Cells

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