scholarly journals Short-chain fatty acids and trichostatin A alter tight junction permeability in human umbilical vein endothelial cells

Nutrition ◽  
2008 ◽  
Vol 24 (11-12) ◽  
pp. 1189-1198 ◽  
Author(s):  
Makoto Miyoshi ◽  
Makoto Usami ◽  
Atsushi Ohata
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Tight Junction ◽  
Trichostatin A ◽  
Umbilical Vein ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Human Umbilical Vein ◽  
Tight Junction Permeability ◽  
Umbilical Vein Endothelial Cells

scholarly journals Turnover of eicosanoid precursor fatty acids among phospholipid classes and subclasses of cultured human umbilical vein endothelial cells

1989 ◽  
Vol 258 (2) ◽  
pp. 427-434 ◽  
Author(s):  
H Takayama ◽  
M H Kroll ◽  
M A Gimbrone ◽  
A I Schafer
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Ionophore A23187 ◽  
Human Umbilical Vein ◽  
Phospholipid Classes ◽  
Specific Increase ◽  
Umbilical Vein Endothelial Cells ◽  
Relationship Of ◽  
The Relationship

Using cultured human umbilical vein endothelial cells, in which phosphatidylcholine (PC) is equally pulse-labelled by various eicosanoid precursor fatty acids (EPFAs), we have studied the remodelling of EPFAs among the phospholipid classes and subclasses with and without activation, and the relationship of this remodelling process to the selective release of arachidonic acid (AA) by phospholipase A2-mediated cell stimulation. When endothelial cells are pulse-incubated with radiolabelled EPFA for 15 min, greater than 80% of cell-associated radioactivity is present in phospholipids, among which greater than 60% is found in 1,2-diacyl-sn-glycero-3-phosphocholine (diacyl PC). After removing unincorporated radioactivity, reincubation of the pulse-labelled cells for up to 6 h results in progressive decrease in EPFA-labelled diacyl PC, increase in AA- or eicosapentaenoic acid (EPA)-labelled 1-O-alk-1-enyl-2-acyl-sn-glycero-3-phosphoethanolamine (plasmalogen PE) and increase only in AA-labelled 1-O-alkyl-2-acyl-sn-glycero-3-phosphocholine (alkyl PC). This redistribution of radiolabelled phospholipids is not altered by the presence of excess non-radiolabelled EPFAs. When aspirin-treated EPFA-labelled endothelial cells are stimulated with ionophore A23187, a very selective release of AA is noted in comparison with eicosatrienoate (ETA) or EPA, accompanied by an equivalent decrease in AA-labelled diacyl PC and specific increase in AA-labelled plasmalogen PE and alkyl PC. These selective changes in AA radioactivity induced by A23187 are enhanced 2-fold by pretreating the AA-labelled cells with phorbol 12-myristate 13-acetate, which by itself induces no changes. The changes in radioactivity induced by A23187 without and with phorbol ester among the released AA, the diacyl PC and the plasmalogen PE are significantly correlated with each other. These results indicate that human endothelial cells incorporate EPFAs (AA, ETA, EPA) equally into diacyl PC but selectively release AA esterified into diacyl PC with specific remodelling into plasmalogen PE and alkyl PC.

scholarly journals Evodiamine Attenuates P2X7-Mediated Inflammatory Injury of Human Umbilical Vein Endothelial Cells Exposed to High Free Fatty Acids

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yun Xue ◽  
Ting Guo ◽  
Lifang Zou ◽  
Yingxin Gong ◽  
Bing Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Endothelial Cells ◽  
Free Fatty Acids ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Umbilical Vein Endothelial Cells

Insulin resistance and type 2 diabetes mellitus (T2DM) are highly prevalent around the world. Elevated concentrations of free fatty acids (FFAs) are closely related to insulin resistance and T2DM. P2X7 receptor is an ion channel gated by ATP, which is implicated in various scenarios including immune response, pain, and inflammation. In this study, we have explored whether P2X7 receptor is involved in pathological changes in human umbilical vein endothelial cells (HUVECs) induced by high FFA treatment, and the potential beneficial effects of evodiamine. Evodiamine could effectively suppress the enhanced expression of P2X7 receptor caused by high FFAs at both mRNA and protein levels. In addition, high FFA-induced cytotoxicity, the upregulated release of ATP, and production of reactive oxygen species (ROS) could be ameliorated by evodiamine in HUVECs. Evodiamine could also reverse the decreased NO formation and the increased adhesive events of immune cells at high FFAs. Moreover, evodiamine inhibited P2X7-dependent TNF-α expression and ERK 1/2 phosphorylation due to high FFAs. All these results indicated that evodiamine could correct the upregulated expression of P2X7 receptor induced under high FFA condition in HUVECs, and consequently suppressed oxidative stress and inflammatory responses.

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