Effect of Hot Water Extracts of White Button Mushrooms on Human Aortic Endothelial Cells (HAEC) Exposed to Hyperglycemia (P06-085-19)

Abstract Objectives In the present study, we investigated the effects of WBM on aortic endothelium alone or in a hyperglycemic environment with or without insulin. Methods Sterile (0.22 um filtered) hot water extracts of WBM (Agaricus bisporus) were added to endothelial basal medium (5% v/v) alone or containing glucose (final concentration 600 mg/dl; 33.3 mM) and/or insulin (100 nM) for 24 hours. Results We show that WBM increased reactive oxygen species (ROS) levels by 2.5-fold (p < 0.05) compared to control cultures using the DCFH-DA assay, which was further increased 18% with insulin inclusion, but decreased by ∼20% in the presence of glucose with or without insulin. WBM also increased nitric oxide (NO) levels by 4-fold (p < 0.05) compared to control cultures, which was further increased by 3.5-fold in the presence of glucose (p < 0.05) suggesting possible potentiation. We noted no differences in NO production, compared to control cultures, with inclusion of insulin with or without glucose. Viability determined by MTT reduction, was not different between any of the groups. Conclusions The results suggest that water-soluble components of WBM may modulate ROS and NO production in a hyperglycemic microenvironment and potentially improve endothelial function, in part, via the potential vasorelaxation properties of NO. Funding Sources Internal Seed Grant, School of Health Studies, University of Memphis, Memphis, TN 38,152.

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Effect of Hot Water Extracts of Maqui Berry on Human Aortic Endothelial Cells Exposed to a Hyperglycemic Environment

Current Developments in Nutrition ◽

10.1093/cdn/nzaa045_068 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 435-435

Author(s):

Keith Martin

Keyword(s):

Endothelial Cells ◽

Endothelial Function ◽

Final Concentration ◽

Water Soluble ◽

Hot Water ◽

No Production ◽

Aortic Endothelial Cells ◽

Maqui Berry ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

Abstract Objectives Impaired endothelial function is associated with many chronic vascular-related diseases including cardiovascular disease, inflammation, and diabetes. The antioxidant-rich Maqui berry (Aristotelia chilensis) has received increasing attention due to a variety of bioactivities including reduction of inflammation, control of blood glucose, and improvement of heart health, e.g., aortic endothelium, but corroborative research is needed. In the present study, we investigated the effects of aqueous Maqui berry extract (MBE) on nitric oxide (NO) production and oxidative stress (ROS) generation in human aortic endothelial cells (HAEC) alone or in a hyperglycemic environment with or without insulin. Methods Sterile (0.22 um filtered) MBE was added to endothelial basal medium (5% v/v) alone or containing glucose (final concentration 600 mg/dL; 33.3 mM) and/or insulin (final concentration 100 nM) followed by addition to monolayers and incubation for 24 hours. Monolayers were then assayed for NO production via the Greiss reaction, ROS via the use of DCFH-DA, and viability using MTT. Results We show that MBE may have increased ROS levels by 1.8-fold (P < 0.05) compared to control cultures using the DCFH-DA assay but decreased by ∼13% in the presence of glucose with or without insulin. MBE also increased NO levels by 3-fold (P < 0.05) compared to levels in control cultures. Glucose inclusion reduced NO by 15% and insulin reduced levels to that of control with or without glucose present. Viability, determined by MTT reduction, was not different between any of the groups. Conclusions The results suggest that water-soluble components of MB may modulate NO production in a hyperglycemic and/or hyperinsulinemic microenvironment and potentially improve endothelial function, in part, via the potential vasorelaxation properties of NO. Funding Sources School of Health Studies, University of Memphis.

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C. pneumoniaedisrupts eNOS trafficking and impairs NO production in human aortic endothelial cells

Cellular Microbiology ◽

10.1111/cmi.12341 ◽

2014 ◽

Vol 17 (1) ◽

pp. 119-130 ◽

Cited By ~ 6

Author(s):

Konrad E. Mueller ◽

Katerina Wolf

Keyword(s):

Endothelial Cells ◽

No Production ◽

Aortic Endothelial Cells ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

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SOME FACTORS AFFECTING THE DETERMINATION OF HOT-WATER-SOLUBLE BORON FROM PODZOL SOILS USING AZOMETHINE-H

Canadian Journal of Soil Science ◽

10.4141/cjss79-027 ◽

1979 ◽

Vol 59 (3) ◽

pp. 241-247 ◽

Cited By ~ 33

Author(s):

UMESH C. GUPTA

Keyword(s):

Prince Edward Island ◽

Sandy Loam ◽

Water Soluble ◽

Hot Water ◽

Colorimetric Determination ◽

Factors Affecting ◽

Water Extracts ◽

Percent Recovery

A study was conducted on some factors affecting the colorimetric determination of B using the azomethine-H reagent on soils from Prince Edward Island. Two fine sandy loam soils (A and B) were used for the main study and additional soil samples varying in organic matter (OM) were used to assess the role of OM. Soils containing less than 3.0% OM and 3.1–4.1% OM required 0.4 g and 0.8 g charcoal per 25 g soil, respectively, to produce clear hot-water extracts. Quantities of greater than 0.8 g charcoal were necessary to produce clear extracts from soils containing more than 4.1% OM. Colored hot-water extracts of soil resulted in higher absorbance than those hot-water extracts treated with charcoal as measured at 430 mμ. Additions of 0.8 and 1.6 g charcoal or greater to the soils (A and B) resulted in considerably lower recoveries of B as noted by comparing the absorbance obtained using 0.4 and 0.8 g, respectively. Storage of azomethine-H up to 7 days did not affect the absorbance of the B-azomethine-H complex. One hour after the addition of azomethine-H, a maximum absorbance was found which persisted for up to 4 h. The percent recovery of B added to the two soils was about 10–12% less using azomethine-H as compared to those obtained using the carmine method. However, the mean hot-water-soluble B contents of 10 soils as measured using the carmine and azomethine-H reagents were 0.70 and 0.66 ppm. Pure B solutions when boiled with charcoal resulted in losses of B added. Such losses of B increased with increasing rates of charcoal.

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Conjugated Metabolites of Hydroxytyrosol and Tyrosol Contribute to the Maintenance of Nitric Oxide Balance in Human Aortic Endothelial Cells at Physiologically Relevant Concentrations

Molecules ◽

10.3390/molecules26247480 ◽

2021 ◽

Vol 26 (24) ◽

pp. 7480

Author(s):

Gabriele Serreli ◽

Melanie Le Sayec ◽

Camilla Diotallevi ◽

Alice Teissier ◽

Monica Deiana ◽

...

Keyword(s):

Nitric Oxide ◽

Endothelial Cells ◽

Leukocyte Adhesion ◽

Virgin Olive Oil ◽

Guanosine Monophosphate ◽

No Production ◽

Aortic Endothelial Cells ◽

Human Aortic Endothelial Cells ◽

Conjugated Metabolites ◽

Aortic Endothelial

Nitric oxide (NO) is an important signaling molecule involved in many pathophysiological processes. NO mediates vasodilation and blood flow in the arteries, and its action contributes to maintaining vascular homeostasis by inhibiting vascular smooth muscle contraction and growth, platelet aggregation, and leukocyte adhesion to the endothelium. Dietary antioxidants and their metabolites have been found to be directly and/or indirectly involved in the modulation of the intracellular signals that lead to the production of NO. The purpose of this study was to investigate the contribution of conjugated metabolites of hydroxytyrosol (HT) and tyrosol (TYR) to the release of NO at the vascular level, and the related mechanism of action, in comparison to their parental forms. Experiments were performed in human aortic endothelial cells (HAEC) to evaluate the superoxide production, the release of NO and production of cyclic guanosine monophosphate (cGMP), the activation of serine/threonine-protein kinase 1 (Akt1), and the activation state of endothelial nitric oxide synthase (eNOS). It was observed that the tested phenolic compounds enhanced NO and cGMP concentration, inhibiting its depletion caused by superoxide overproduction. Moreover, some of them enhanced the activation of Akt (TYR, HT metabolites) and eNOS (HT, HVA, TYR-S, HT-3S). Overall, the obtained data showed that these compounds promote NO production and availability, suggesting that HT and TYR conjugated metabolites may contribute to the effects of parental extra virgin olive oil (EVOO) phenolics in the prevention of cardiovascular diseases.

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Phytoestrogen Genistein Up-Regulates Endothelial Nitric Oxide Synthase Expression Via Activation of cAMP Response Element-Binding Protein in Human Aortic Endothelial Cells

Endocrinology ◽

10.1210/en.2012-1076 ◽

2012 ◽

Vol 153 (7) ◽

pp. 3190-3198 ◽

Cited By ~ 15

Author(s):

Hongwei Si ◽

Jie Yu ◽

Hongling Jiang ◽

Hazel Lum ◽

Dongmin Liu

Keyword(s):

Nitric Oxide ◽

Endothelial Cells ◽

Endothelial Nitric Oxide Synthase ◽

No Production ◽

Enos Expression ◽

Camp Response Element ◽

Aortic Endothelial Cells ◽

Oxide Synthase ◽

Endothelial Nitric Oxide ◽

Human Aortic Endothelial Cells

We previously reported that genistein, a phytoestrogen, up-regulates endothelial nitric oxide synthase (eNOS) and prevents hypertension in rats that are independent of estrogen signaling machinery. However, how genistein regulates eNOS expression is unknown. In the present study, we show that genistein enhanced eNOS expression and NO synthesis in primary human aortic endothelial cells. Inhibition of extracellular signal regulated kinase, phosphoinositol-3 kinase, or protein kinase C did not affect genistein-enhanced eNOS expression and NO synthesis. However, chemical inhibition of protein kinase A (PKA) or adenoviral transfer of the specific endogenous PKA inhibitor gene completely abolished PKA activity and genistein-stimulated eNOS expression and NO production. Accordingly, genistein induced PKA activity and subsequent phosphorylation of cAMP response element (CRE)-binding protein (CREB) at Ser133. Suppression of CREB by small interfering RNA transfection abolished genistein-enhanced eNOS expression and NO production. Consistently, deletion of the CRE site within human eNOS promoter eliminated genistein-stimulated eNOS promoter activity. These findings provide the first evidence to our knowledge that genistein may play a beneficial role in vascular function through targeting the PKA/CREB/eNOS/NO signaling pathway.

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Enhancement of the Anti-Angiogenic Effects of Delphinidin When Encapsulated within Small Extracellular Vesicles

Nutrients ◽

10.3390/nu13124378 ◽

2021 ◽

Vol 13 (12) ◽

pp. 4378

Author(s):

Merwan Barkallah ◽

Judith Nzoughet-Kouassi ◽

Gilles Simard ◽

Loric Thoulouze ◽

Sébastien Marze ◽

...

Keyword(s):

Extracellular Vesicle ◽

No Production ◽

Proliferation Assay ◽

Aortic Endothelial Cells ◽

Immature Dendritic Cells ◽

Endothelial Proliferation ◽

The Stability ◽

Human Aortic Endothelial Cells

(1) Background: The anthocyanin delphinidin exhibits anti-angiogenic properties both in in vitro and in vivo angiogenesis models. However, in vivo delphinidin is poorly absorbed, thus its modest bioavailability and stability reduce its anti-angiogenic effects. The present work takes advantage of small extracellular vesicle (sEV) properties to enhance both the stability and efficacy of delphinidin. When encapsulated in sEVs, delphinidin inhibits the different stages of angiogenesis on human aortic endothelial cells (HAoECs). (2) Methods: sEVs from immature dendritic cells were produced and loaded with delphinidin. A method based on UHPLC-HRMS was implemented to assess delphinidin metabolites within sEVs. Proliferation assay, nitric oxide (NO) production and Matrigel assay were evaluated in HAoECs. (3) Results: Delphinidine, 3-O-β-rutinoside and Peonidin-3-galactoside were found both in delphinidin and delphinidin-loaded sEVs. sEV-loaded delphinidin increased the potency of free delphinidin 2-fold for endothelial proliferation, 10-fold for endothelial NO production and 100-fold for capillary-like formation. Thus, sEV-loaded delphinidin exerts effects on the different steps of angiogenesis. (4) Conclusions: sEVs may be considered as a promising approach to deliver delphinidin to target angiogenesis-related diseases, including cancer and pathologies associated with excess vascularization.

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Globular adiponectin counteracts VCAM-1-mediated monocyte adhesion via AdipoR1/NF-κB/COX-2 signaling in human aortic endothelial cells

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00208.2011 ◽

2011 ◽

Vol 301 (6) ◽

pp. E1143-E1154 ◽

Cited By ~ 30

Author(s):

Francesco Addabbo ◽

Carmela Nacci ◽

Leonarda De Benedictis ◽

Valentina Leo ◽

Mariela Tarquinio ◽

...

Keyword(s):

Endothelial Cells ◽

Biological Activities ◽

Biological Properties ◽

No Production ◽

Monocyte Adhesion ◽

Aortic Endothelial Cells ◽

Cox 2 ◽

Activated Monocytes ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

Adiponectin (Ad) is an insulin-sensitizing adipocytokine with anti-inflammatory and vasoprotective properties. Cleavage of native full-length Ad (fAd) by elastases from activated monocytes generates globular Ad (gAd). Increased gAd levels are observed in the proximity of atherosclerotic lesions, but the physiological meaning of this proteolytic Ad fragment in the cardiovascular system is controversial. We compared molecular and biological properties of fAd and gAd in human aortic endothelial cells (HAEC). In control HAEC, both fAd and gAd acutely stimulated nitric oxide (NO) production by AMPK-dependent pathways. With respect to fAd, gAd more efficiently increased activation of NF-κB signaling pathways, resulting in cyclooxygenase-2 (COX-2) overexpression and COX-2-dependent prostacyclin 2 (PGI2) release. In contrast with fAd, gAd also increased p38 MAPK phosphorylation and VCAM-1 expression, ultimately enhancing adhesion of monocytes to endothelial cells. In HAEC lacking AdipoR1 (by siRNA), both activation of NF-κB as well as COX-2 overexpression by gAd were abrogated. Conversely, gAd-mediated p38MAPK activation and VCAM-1 expression were unaffected, and monocyte adhesion was greatly enhanced. In HAEC lacking COX-2 (by siRNA), reduced levels of PGI2 further increased gAd-dependent monocyte adhesion. Our findings suggest that biological activities of fAd and gAd in endothelium do not completely overlap, with gAd possessing both AdipoR1-dependent ability to stimulate COX-2 expression and AdipoR1-independent effects related to expression of VCAM-1 and adhesion of monocytes to endothelium.

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