scholarly journals Potent Stimulation of Blood Flow in Fingers of Volunteers after Local Short-Term Treatment with Low-Frequency Magnetic Fields from a Novel Device

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Richard H. W. Funk ◽  
Lilla Knels ◽  
Antje Augstein ◽  
Rainer Marquetant ◽  
Hermann F. Dertinger
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Endothelial Cells ◽  
Low Frequency ◽  
Rapid Onset ◽  
Term Treatment ◽  
No Production ◽  
Vascular Endothelial ◽  
Short Term Treatment ◽  
Novel Device

A novel hand-held low-frequency magnetic stimulator (MagCell-SR) was tested for its ability to stimulate microcirculation in fingers of healthy volunteers. Blood flow during and after 5 minutes exposure was quantified using Laser Doppler Perfusion Imaging Technique. The device was positioned between the wrist and the dorsal part of the backhand. Because the increase in blood flow could be caused by a release of nitric oxide (NO) from the vascular endothelial cells we tested NO production with a fluorescence marker and quantified the measurements in cell cultures of human umbilical endothelial cells (HUVEC). Exposure increased blood flow significantly, persisted several minutes, and then disappeared gradually. In order to assess the effect of a static magnetic field, the measurements were also carried out with the device shutoff. Here, only a small increase in blood flow was noted. The application of the rotating MagCell-SR to the HUVEC cultures leads to a rapid onset and a significant increase of NO release after 15 minutes. Thus, frequencies between 4 and 12 Hz supplied by the device improve microcirculation significantly. Therefore, this device can be used in all clinical situations where an improvement of the microcirculation is useful like in chronic wound healing deficits.

Hydroxytyrosol NO regulates oxidative stress and NO production through SIRT1 in diabetic mice and vascular endothelial cells

Phytomedicine ◽  
2019 ◽  
Vol 52 ◽  
pp. 206-215 ◽  
Author(s):  
Weirong Wang ◽  
Chenxu Shang ◽  
Wei Zhang ◽  
Zhen Jin ◽  
Feng Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
No Production ◽  
Vascular Endothelial ◽  
Diabetic Mice

scholarly journals Bile Acid Receptor TGR5 Agonism Induces NO Production and Reduces Monocyte Adhesion in Vascular Endothelial Cells

2013 ◽  
Vol 33 (7) ◽  
pp. 1663-1669 ◽  
Author(s):  
Taiki Kida ◽  
Yoshiki Tsubosaka ◽  
Masatoshi Hori ◽  
Hiroshi Ozaki ◽  
Takahisa Murata
Keyword(s):  
Endothelial Cells ◽  
Bile Acid ◽  
Vascular Endothelial Cells ◽  
No Production ◽  
Vascular Endothelial ◽  
Monocyte Adhesion ◽  
Acid Receptor ◽  
Bile Acid Receptor

Abstract 153: Bile Acid Receptor TGR5 Agonism Represents Anti-inflammatory Effects via Stimulating Nitric Oxide Production in Vascular Endothelial Cells

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Taiki Kida ◽  
Yoshiki Tsubosaka ◽  
Masatoshi Hori ◽  
Hiroshi Ozaki ◽  
Takahisa Murata
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Bile Acids ◽  
Inflammatory Responses ◽  
Vascular Endothelial Cells ◽  
Lithocholic Acid ◽  
Signal Pathways ◽  
No Production ◽  
Vascular Endothelial ◽  
Anti Inflammatory

Objective TGR5, a membrane-bound, G-protein-coupled receptor for bile acids, is known to be involved in regulation of energy homeostasis and inflammation. However, little is known about the function of TGR5 in vascular endothelial cells. In the present study, we examined whether TGR5 agonism represents anti-inflammatory effects in vascular endothelial cells focusing on nitric oxide (NO) production. Methods and Results In human umbilical vein endothelial cells (HUVECs), treatment with taurolithocholic acid (TLCA), which has the highest affinity to TGR5 among various bile acids, significantly reduced tumor necrosis factor (TNF)-α-induced vascular cell adhesion molecule (VCAM)-1 protein expression and adhesion of human monocytes, U937. These effects were abrogated by a NO synthase (NOS) inhibitor, N G -Monomethyl-L-arginine (L-NMMA). In bovine aortic endothelial cells (BAECs), treatment with TLCA as well as lithocholic acid, which also has high affinity to TGR5, significantly increased the NO production. In contrast, deoxycholic acid and chenodeoxycholic acid, which possess low affinity to TGR5, did not affect the NO production. Gene depletion of TGR5 by siRNA transfection abolished TLCA-induced NO production in BAECs. TLCA-induced NO production was also observed in HUVECs measured as intracellular cGMP accumulation. We next investigated the signal pathways responsible for the TLCA-induced NO production in endothelial cells. Treatment with TLCA increased endothelial NOS (eNOS) ser1177 phosphorylation in HUVECs. This response was accompanied by increased Akt ser473 phosphorylation and intracellular Ca 2+ ([Ca 2+ ] i ). Treatment with phosphoinositide 3-kinase (PI3K) inhibitor, LY294002, or blockade of calcium channel with La 3+ , significantly decreased TLCA-induced eNOS ser1177 phosphorylation and subsequent NO production. Conclusion These results indicate that TGR5 agonism can mediate anti-inflammatory responses by suppressing VCAM-1 expression and monocytes adhesion to endothelial cells. This function is dependent on NO production via Akt activation and [Ca 2+ ] i increase.

scholarly journals Mechanosensing of blood flow in vascular endothelial cells

2011 ◽  
Vol 138 (5) ◽  
pp. 196-200 ◽  
Author(s):  
Kimiko Yamamoto ◽  
Joji Ando
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Disturbed flow: p53 SUMOylation in the turnover of endothelial cells

2011 ◽  
Vol 193 (5) ◽  
pp. 805-807 ◽  
Author(s):  
Wakako Takabe ◽  
Noah Alberts-Grill ◽  
Hanjoong Jo
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Protein Inhibitor ◽  
Disturbed Flow ◽  
Antiapoptotic Protein ◽  
Kinase C

Disturbed blood flow induces apoptosis of vascular endothelial cells, which causes atherosclerosis. In this issue, Heo et al. (2011. J. Cell Biol. doi:10.1083/jcb.201010051) sheds light on p53’s role in this phenomenon. Disturbed flow induces peroxynitrite production, which activates protein kinase C ζ and it’s binding to the E3 SUMO (small ubiquitin-like modifier) ligase PIASy (protein inhibitor of activated STATy). This leads to p53 SUMOylation and its export to the cytosol, where it binds to the antiapoptotic protein Bcl-2 to induce apoptosis.

Abstract 221: The P2x4 Receptor is Required for Neuroprotection via Ischemic Preconditioning

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Tomohiko Ozaki ◽  
Rieko Muramatsu ◽  
Toshiyuki Fujinaka ◽  
Toshiki Yoshimine ◽  
Toshihide Yamashita
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Endothelial Cells ◽  
Ischemic Tolerance ◽  
Receptor Expression ◽  
Vascular Endothelial ◽  
P2x4 Receptor ◽  
Flow Changes

Background: Ischemic preconditioning (IPC), a procedure consisting of transient ischemia and subsequent reperfusion, provides ischemic tolerance against prolonged ischemia in the brain. Although the blood flow changes mediated by IPC are primarily perceived by vascular endothelial cells, the role of these cells in ischemic tolerance has not fully clarified. In this research, we focused on the role of P2X4 receptor, which sense blood flow changes and is expressed on vascular endothelial cells. Methods: We administrated P2X4 receptor inhibitor into lateral ventricle of C57BL/6J male mice (8-10 weeks) and then conducted middle cerebral artery occlusion (MCAO). Fifteen minutes MCAO was done as IPC 48 hours before 60 minutes MCAO. To examine the necessity of P2X4 receptor expression in vascular endothelial cells, we generated a conditional knockout (CKO) mouse in which the P2X4 receptor was knocked down in VE-cadherin-positive vascular endothelial cells. To investigate molecular change by IPC, we obtained cerebrovascular endothelial cells of mice 48 hours after IPC, and real time PCR and ELISA were evaluated. To examine the molecular expression change on vascular endothelial cells by blood flow, we used in vitro culture system which generates fluid flow and real time PCR was evaluated. Inhibition of P2X4 receptor expression was conducted by P2X4 receptor siRNA transfection. Results: P2X4 receptor antagonist abolished neuroprotection via IPC. Moreover, the effect of IPC to P2X4 receptor CKO mice was smaller than control mice, the infarct volume of P2X4 receptor CKO was larger than control mice after 60 minutes MCAO (p<0.05, Control, n=4; CKO, n=6). IPC induced expression of osteopontin mRNA (p<0.05, n=5). Osteopontin administration attenuates the increase of infarct formation induced by P2X4 receptor inhibition (p<0.05, Control, n=5; Osteopontin, n=6). In vitro, shear stress upregulated expression of osteopontin mRNA (p<0.05, n=3). This upregulation was inhibited by P2X4 receptor siRNA (p<0.05, Control siRNA, n=6; P2X4 receptor siRNA, n=7). Conclusion: These results demonstrate a novel mechanism whereby vascular endothelial cells are involved in ischemic tolerance by way of the pathway about P2X4 receptor and osteopontin.

scholarly journals Black soybean seed coat polyphenols promote nitric oxide production in the aorta through the Akt/eNOS pathway

2020 ◽  
Vol 10 (8) ◽  
pp. 330
Author(s):  
Chiaki Domae ◽  
Hitoshi Ashida ◽  
Yoko Yamashita
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Seed Coat ◽  
Vascular Endothelial Cells ◽  
Soybean Seed ◽  
No Production ◽  
Vascular Endothelial ◽  
Intestinal Epithelial ◽  
Black Soybean ◽  
Soybean Seed Coat

Background: Black soybean seed coat contains an abundance of flavan-3-ols and possesses various bioregulatory functions. Nitric oxide (NO) is produced by endothelial nitric oxide synthase (eNOS) in vascular endothelial cells and regulates vascular function through vasodilation and the inhibition of platelet aggregation in blood vessels. It has been reported that flavan-3-ols increase NO production, but many previous reports used a high concentration of flavan-3-ols. In the present study, we investigated the effect of flavan-3-ol-rich black soybean seed coat extract (BE) on NO production at a lower concentration that is close to the concentration after permeation through the monolayer of Caco-2 cells.Methods: Human umbilical vein endothelial cells (HUVEC) were incubated with BE, and then NO production in the medium and eNOS phosphorylation in the cells were examined. Intestinal epithelial Caco-2 cells on the upper side of a transwell filter were co-cultured with HUVEC on the basolateral compartment of the transwell apparatus. BE was added from the upper side, and the basolateral medium was collected to measure the concentration of NO and the content of flavan-3-ols. Furthermore, HUVEC were incubated with each flavan-3-ol in order to individuate the most effective compound in BE.Results: BE significantly increased NO production in the medium of HUVEC. When polyphenols in BE were removed from the basolateral medium by ethyl acetate extraction, increased NO production from HUVEC was not observed. Additionally, BE increased phosphorylation of eNOS and Akt in HUVEC. A portion of flavan-3-ols in BE had permeated through intestinal epithelial cells. Among the flavan-3-ols that had permeated, procyanidin C1 had the strongest effect on NO production in HUVEC at the concentration that had permeated the monolayer of Caco-2 cells. Procyanidin C1 (0.05 µM) also induced phosphorylation of eNOS and Akt in HUVEC without affecting the cAMP level. Conclusion: A portion of flavan-3-ols in BE directly promoted NO production through the Akt/eNOS pathway in vascular endothelial cells. These findings suggest that flavan-3-ols in the black soybean seed coat may contribute to improve the vascular function.Keywords: Black soybean seed coat polyphenols; NO; eNOS; Akt; vascular endothelial cells

Distinct Ca2+ Requirement for NO Production between Proteinase-Activated Receptor 1 and 4 (PAR1 and PAR4) in Vascular Endothelial Cells

2007 ◽  
Vol 322 (2) ◽  
pp. 668-677 ◽  
Author(s):  
Katsuya Hirano ◽  
Namie Nomoto ◽  
Mayumi Hirano ◽  
Fumi Momota ◽  
Akiko Hanada ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
No Production ◽  
Vascular Endothelial

EFFECTS OF LOW-FREQUENCY ELECTRIC FIELDS ON THE INTRACELLULAR Ca2+RESPONSE INDUCED IN HUMAN VASCULAR ENDOTHELIAL CELLS BY VASOACTIVE SUBSTANCES

2002 ◽  
Vol 21 (3) ◽  
pp. 279-286 ◽  
Author(s):  
Kunihito Takahashi ◽  
Masahiko Kuroki ◽  
Fuyuki Doge ◽  
Yoshio Sawasaki ◽  
Masahiko Yoshioka
Keyword(s):  
Endothelial Cells ◽  
Electric Fields ◽  
Vascular Endothelial Cells ◽  
Low Frequency ◽  
Vascular Endothelial ◽  
Vasoactive Substances
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