scholarly journals Resveratrol blocks atherosclerosis development by inhibiting IL-1β in macrophages induced by cholesterol

2019 ◽  
Vol 71 (3) ◽  
pp. 551-559
Author(s):  
Yilin Xie ◽  
Zhaoxia Wang ◽  
Haiyun Lin ◽  
Yajun Pan ◽  
Lianyun Wang ◽  
...  
Keyword(s):  
Umbilical Vein ◽  
Protective Role ◽  
Expression Level ◽  
Cell Culture Supernatant ◽  
Caveolin 1 ◽  
Cholesterol Treatment ◽  
Atherosclerosis Development ◽  
Umbilical Vein Endothelial Cells ◽  
Antiinflammatory Effects

Resveratrol is a polyphenolic compound that exhibits antiinflammatory and cardioprotective properties. In this study we investigated the protective role of resveratrol on the inflammatory activation of macrophages during pathogenesis of atherosclerosis. Macrophage Ana-1 cells were stimulated by cholesterol and resveratrol, and the cell culture supernatant was collected to treat human umbilical vein endothelial cells (HUVECs). The release of IL-1? into the Ana-1 cell supernatant was quantified by ELISA. Expression of the adhesion molecule ICAM-1 and E-selectin in HUVECs were examined by Western-blotting. Additionally, the adhesion of monocytes in HUVECs under different conditions was tested by cell adhesion analyses. The results indicated that the high cholesterol treatment increased the expression level of IL-1?, while pretreatment with resveratrol inhibited this induction of IL-1? in Ana-1 cells. Resveratrol inhibited the adhesion of monocytes to the endothelium at least partly through inhibition of IL-1? expression in macrophages. Moreover, the expression level of caveolin-1 significantly increased after the pretreatment with resveratrol, indicating that resveratrol enhances reverse cholesterol transport (RCT) in macrophages. Our study indicated that resveratrol has significant antiinflammatory effects and can be considered as a candidate molecule to prevent atherosclerosis.

scholarly journals The role of miR-146a on NF-κB expression level in human umbilical vein endothelial cells under hyperglycemic condition

2016 ◽  
Vol 117 (07) ◽  
pp. 376-380 ◽  
Author(s):  
K. Kamali ◽  
E. Salmani Korjan ◽  
E. Eftekhar ◽  
K. Malekzadeh ◽  
F. Ghadiri Soufi
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Expression Level ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals A Protective Role of Paeoniflorin in Fluctuant Hyperglycemia-Induced Vascular Endothelial Injuries through Antioxidative and Anti-Inflammatory Effects and Reduction of PKCβ1

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jing-Shang Wang ◽  
Ye Huang ◽  
Shuping Zhang ◽  
Hui-Jun Yin ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Umbilical Vein ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Glucose Levels ◽  
Umbilical Vein Endothelial Cells

Hyperglycemia fluctuation is associated with diabetes mellitus (DM) complications when compared to persistent hyperglycemia. Previous studies have shown that paeoniflorin (PF), through its antiapoptosis, anti-inflammation, and antithrombotic properties, effectively protects against cardiovascular and cerebrovascular disease. However, the mechanism underlying the protection from PF against vascular injuries induced by hyperglycemia fluctuations remains poorly understood. Herein, we investigated the potential protective role of PF on human umbilical vein endothelial cells (HUVECs) subjected to intermittent glucose levels in vitro and in DM rats with fluctuating hyperglycemia in vivo. A remarkable increased apoptosis associated with elevated inflammation, increased oxidative stress, and high protein level of PKCβ1 was induced in HUVECs by intermittently changing glucose for 8 days, and PF recovered those detrimental changes. LY333531, a potent PKCβ1 inhibitor, and metformin manifested similar effects. Additionally, in DM rats with fluctuating hyperglycemia, PF protected against vascular damage as what has been observed in vitro. Taken together, PF attenuates the vascular injury induced by fluctuant hyperglycemia through oxidative stress inhibition, inflammatory reaction reduction, and PKCβ1 protein level repression, suggesting its perspective clinical usage.

scholarly journals The Impact of Simulated Weightlessness on Endothelium-Dependent Angiogenesis and the Role of Caveolae/Caveolin-1

2016 ◽  
Vol 38 (2) ◽  
pp. 502-513 ◽  
Author(s):  
Fei Shi ◽  
Tian-Zhi Zhao ◽  
Yong-Chun Wang ◽  
Xin-Sheng Cao ◽  
Chang-Bin Yang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Microgravity Environment ◽  
Caveolin 1 ◽  
Endothelial Functions ◽  
Umbilical Vein Endothelial Cells ◽  
The Impact

Background/Aims: The potential role of caveolin-1 in modulating angiogenesis in microgravity environment is unexplored. Methods: Using simulated microgravity by clinostat, we measured the expressions and interactions of caveolin-1 and eNOS in human umbilical vein endothelial cells. Results: We found that decreased caveolin-1 expression is associated with increased expression and phosphorylation levels of eNOS in endothelial cells stimulated by microgravity, which causes a dissociation of eNOS from caveolin-1 complexes. As a result, microgravity induces cell migration and tube formation in endothelial cell in vitro that depends on the regulations of caveolin-1. Conclusion: Our study provides insight for the important endothelial functions in altered gravitational environments.

Vascular Protective Role of Vitexicarpin Isolated from Vitex rotundifolia in Human Umbilical Vein Endothelial Cells

Inflammation ◽  
2011 ◽  
Vol 35 (2) ◽  
pp. 584-593 ◽  
Author(s):  
So Min Lee ◽  
Yun Jung Lee ◽  
Youn Chul Kim ◽  
Jin Sook Kim ◽  
Dae Gill Kang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Protective Role ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Thrombin Augments Vascular Cell-dependent Migration of Human Mast Cells: Role of MGF

1997 ◽  
Vol 77 (03) ◽  
pp. 577-584 ◽  
Author(s):  
Mehrdad Baghestanian ◽  
Roland Hofbauer ◽  
Hans G Kress ◽  
Johann Wojta ◽  
Astrid Fabry ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mast Cells ◽  
Umbilical Vein ◽  
Vascular Cells ◽  
Migratory Response ◽  
Thrombin Activation ◽  
Umbilical Vein Endothelial Cells ◽  
Primary Tissue ◽  
Local Expression

SummaryRecent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

scholarly journals Lipid Emulsion Enhances Vasoconstriction Induced by Dexmedetomidine in the Isolated Endothelium-Intact Aorta

2021 ◽  
Vol 22 (7) ◽  
pp. 3309
Author(s):  
Soo Hee Lee ◽  
Seong-Ho Ok ◽  
Seung Hyun Ahn ◽  
Hyun-Jin Kim ◽  
Sung Il Bae ◽  
...  
Keyword(s):  
Lipid Emulsion ◽  
Umbilical Vein ◽  
Src Kinase ◽  
Cyclic Guanosine Monophosphate ◽  
Rat Aorta ◽  
Guanosine Monophosphate ◽  
Caveolin 1 ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Nitric Oxide ◽  
Cgmp Formation

This study aimed to examine the effect of lipid emulsion (LE) on the vasoconstriction induced by dexmedetomidine (DMT) in the isolated rat aorta and elucidate the associated cellular mechanism. The effect of LE, NW-nitro-L-arginine methyl ester (L-NAME), and methyl-β-cyclodextrin (MβCD) on the DMT-induced contraction was examined. We investigated the effect of LE on the DMT-induced cyclic guanosine monophosphate (cGMP) formation and DMT concentration. The effect of DMT, LE, 4-Amino-3-(4-chlorophenyl)-1-(t-butyl)-1H-pyrazolo[3,4-d]pyrimidine,4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), and rauwolscine on the phosphorylation of endothelial nitric oxide synthase (eNOS), caveolin-1, and Src kinase was examined in the human umbilical vein endothelial cells. L-NAME, MβCD, and LE (1%, standardized mean difference (SMD): 2.517) increased the DMT-induced contraction in the endothelium-intact rat aorta. LE (1%) decreased the DMT (10−6 M) concentration (SMD: −6.795) and DMT-induced cGMP formation (SMD: −2.132). LE (1%) reversed the DMT-induced eNOS (Ser1177 and Thr496) phosphorylation. PP2 inhibited caveolin-1 and eNOS phosphorylation induced by DMT. DMT increased the Src kinase phosphorylation. Thus, LE (1%) enhanced the DMT-induced contraction by inhibition of NO synthesis, which may be caused by the decreased DMT concentration. DMT-induced NO synthesis may be caused by the increased eNOS (Ser1177) phosphorylation and decreased eNOS (Thr495) phosphorylation potentially mediated by Src kinase-induced caveolin-1 phosphorylation.

scholarly journals SiRNA Directed Against Annexin II Receptor Inhibits Angiogenesis via Suppressing MMP2 and MMP9 Expression

2015 ◽  
Vol 35 (3) ◽  
pp. 875-884 ◽  
Author(s):  
Hongyuan Song ◽  
Dongyan Pan ◽  
Weifeng Sun ◽  
Cao Gu ◽  
Yuelu Zhang ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Annexin Ii ◽  
Mmp9 Expression ◽  
Cell Arrest ◽  
Umbilical Vein Endothelial Cells

Background/Aims: Annexin II receptor (AXIIR) is able to mediate Annexin II signal and induce apoptosis, but its role in angiogenesis remains unclear. This study tries to investigate the role of AXIIR in angiogenesis and the plausible molecular mechanism. Methods/Results: RNA interference technology was used to silence AXIIR, and the subsequent effects in vitro and in vivo were evaluated thereafter. Our data indicated that human umbilical vein endothelial cells (HUVECs) expressed AXIIR and knockdown of AXIIR significantly inhibited HUVECs proliferation, adhesion, migration, and tube formation in vitro and suppressed angiogenesis in vivo. Furthermore, AXIIR siRNA induced cell arrest in the S/G2 phase while had no effect on cell apoptosis. We found that these subsequent effects might be via suppressing the expression of matrix metalloproteinase 2and matrix metalloproteinase 9. Conclusion: AXIIR participates in angiogenesis, and may be a potential therapeutic target for angiogenesis related diseases.

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