scholarly journals Punicalagin Induce the Production of Nitric Oxide and Inhibit Angiotensin Converting Enzyme in Endothelial Cell Line EA.hy926

2016 ◽  
Vol 4 (5) ◽  
pp. 268-277 ◽  
Author(s):  
Ulfat Omar ◽  
Akram Aloqbi ◽  
Marwa Yousr ◽  
Nazlin K. Howell
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Angiotensin Converting Enzyme ◽  
Cell Line ◽  
Converting Enzyme ◽  
Endothelial Cell Line

scholarly journals Arachidonic Acid Evokes an Increase in Intracellular Ca2+ Concentration and Nitric Oxide Production in Endothelial Cells from Human Brain Microcirculation

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 689 ◽  
Author(s):  
Roberto Berra-Romani ◽  
Pawan Faris ◽  
Sharon Negri ◽  
Laura Botta ◽  
Tullio Genova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
Endothelial Cell ◽  
Human Brain ◽  
Cell Line ◽  
Transient Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Cerebral Microvessels ◽  
Endothelial Cell Line ◽  
No Release

It has long been known that the conditionally essential polyunsaturated arachidonic acid (AA) regulates cerebral blood flow (CBF) through its metabolites prostaglandin E2 and epoxyeicosatrienoic acid, which act on vascular smooth muscle cells and pericytes to vasorelax cerebral microvessels. However, AA may also elicit endothelial nitric oxide (NO) release through an increase in intracellular Ca2+ concentration ([Ca2+]i). Herein, we adopted Ca2+ and NO imaging, combined with immunoblotting, to assess whether AA induces intracellular Ca2+ signals and NO release in the human brain microvascular endothelial cell line hCMEC/D3. AA caused a dose-dependent increase in [Ca2+]i that was mimicked by the not-metabolizable analogue, eicosatetraynoic acid. The Ca2+ response to AA was patterned by endoplasmic reticulum Ca2+ release through type 3 inositol-1,4,5-trisphosphate receptors, lysosomal Ca2+ mobilization through two-pore channels 1 and 2 (TPC1-2), and extracellular Ca2+ influx through transient receptor potential vanilloid 4 (TRPV4). In addition, AA-evoked Ca2+ signals resulted in robust NO release, but this signal was considerably delayed as compared to the accompanying Ca2+ wave and was essentially mediated by TPC1-2 and TRPV4. Overall, these data provide the first evidence that AA elicits Ca2+-dependent NO release from a human cerebrovascular endothelial cell line, but they seemingly rule out the possibility that this NO signal could acutely modulate neurovascular coupling.

scholarly journals Myricetin inhibits angiotensin converting enzyme and induces nitric oxide production in HUVEC cell line

2020 ◽  
Vol 39 (03) ◽  
pp. 249-258
Author(s):  
Mehmet Berköz ◽  
Metin Yıldırım ◽  
Serap Yalın ◽  
Mert İlhan ◽  
Oruç Yunusoğlu
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Converting Enzyme ◽  
Cell Line ◽  
Nitric Oxide Production ◽  
Converting Enzyme ◽  
Oxide Production ◽  
Huvec Cell

scholarly journals Endothelial and Vascular Health: A Tale of Honey, H2O2 and Calcium

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1071
Author(s):  
Elia Ranzato ◽  
Gregorio Bonsignore ◽  
Mauro Patrone ◽  
Simona Martinotti
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Line ◽  
Cellular Responses ◽  
Pivotal Role ◽  
Vascular Health ◽  
Endothelial Cell Line ◽  
Positive Effects

Intracellular Ca2+ regulation plays a pivotal role in endothelial biology as well as during endothelial restoration processes. Interest in honey utilization in wound approaches is rising in recent years. In order to evaluate the positive effects of buckwheat honey on endothelial responses, we utilized an immortalized endothelial cell line to evaluate cellular responses upon honey exposure, with particular interest in Ca2+ signaling involvement. The results highlight the positive effects of buckwheat honey on endothelial cells’ responses and the central role played by Ca2+ signaling as an encouraging target for more efficacious clinical treatments.

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