FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2901848907> ?p ?o ?g. }

• W2901848907 abstract "Ischemia/reperfusion (I/R) injury plays a critical role in endothelial dysfunction as a consequence of limited nitric oxide (NO) bioavailability and excess generation of reactive oxygen species (ROS) generated by endothelial nitric oxide synthase (eNOS) during reperfusion. Activated protein kinase C epsilon (PKCɛ) binds to a specific receptor for activated C kinase (RACK-1), facilitating its translocation from the cytosol to the cell membrane for phosphorylation of targets, such as eNOS, at serine-1177 to augment activity. Previous in vitro and in vivo animal studies have shown that PKCɛ activation stimulates eNOS activity, increasing NO release; whereas PKCɛ inhibition using a peptide inhibitor that interferes with its interaction with RACK-1 results in decreased NO release. However, the modulation of PKCɛ-mediated eNOS activity has yet to be demonstrated in human cells. In this study, we aim to demonstrate enhancement and attenuation of NO release in human umbilical vein endothelial cells (HUVECs) using cell-permeable, myristic-acid conjugated PKCɛ activator (Myr-PKCɛ+), Myr-HDAPIGYD (MW=1097 g/mol), and inhibitor (Myr-PKCɛ−), Myr-EAVSLKPT (MW=1054 g/mol), peptides respectively. Single-donor HUVECs at passages 3–4 were grown to confluence in 6-well (35 mm) plates. NO release was measured in real time using a calibrated NO electrode following the administration of 10 μM Myr-PKCɛ+ or 10 μM Myr-PKCɛ− treatments in the absence or presence of 10 μM acetylcholine (Ach) stimulation of NO release. Basal NO release (375±175 pM) was determined by measuring the difference between wells with and without cells (n=4). Myr-PKCɛ+ increased NO levels by 36±13 pM (p<0.01, n=5) and Myr-PKCɛ− decreased NO levels by 41±55 pM, p<0.01, n=5) significantly compared to baseline in the absence of Ach stimulation. In the presence of 10 μM Ach only, NO release significantly increased by 61±15 pM above baseline (p<0.01, n=5). In Ach-stimulated cells, there was an additional significant increase in NO release by 70±23 pM (p<0.01, n=5) when treated with Myr-PKCɛ+ compared to baseline, although there was no significance compared to the initial Ach-stimulated NO release. Following initial 10 μM Ach administration, Myr-PKCɛ− significantly reduced NO release by 48±16 pM, (p<0.01, n=5) compared to baseline. These results suggest Myr-PKCɛ+ presumably increases NO release via activation of eNOS, whereas Myr-PKCɛ− attenuates eNOS activity by inhibiting its phosphorylation in HUVECs; thus, eNOS modulation by these peptides demonstrate comparable effects across species. Elucidating the role of eNOS modulation is important for developing therapeutic interventions in the context of human organ I/R injury, in which uncoupled eNOS produces ROS instead of NO. Future studies will evaluate the effects of Myr-PKCɛ+ and Myr-PKCɛ− on NO release in HUVECs during reperfusion following prolonged ischemia compared to non-ischemic controls. Support or Funding Information This study was supported by the Center for Chronic Disorders of Aging, the Division of Research and the Department of Biomedical Sciences at Philadelphia College of Osteopathic Medicine. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
• W2901848907 created "2018-11-29" @default.
• W2901848907 creator A5006204901 @default.
• W2901848907 creator A5007579766 @default.
• W2901848907 creator A5023102915 @default.
• W2901848907 creator A5061337633 @default.
• W2901848907 creator A5063018006 @default.
• W2901848907 creator A5068290128 @default.
• W2901848907 creator A5088089771 @default.
• W2901848907 creator A5091712727 @default.
• W2901848907 date "2018-04-01" @default.
• W2901848907 modified "2023-09-24" @default.
• W2901848907 title "Modulation of Nitric Oxide Release in Human Umbilical Vein Endothelial Cells by Myristolated‐PKC Epsilon Activator/Inhibitor Peptides" @default.
• W2901848907 cites W1984668546 @default.
• W2901848907 cites W2012978268 @default.
• W2901848907 cites W2326703339 @default.
• W2901848907 cites W3171502915 @default.
• W2901848907 doi "https://doi.org/10.1096/fasebj.2018.32.1_supplement.902.19" @default.
• W2901848907 hasPublicationYear "2018" @default.
• W2901848907 type Work @default.
• W2901848907 sameAs 2901848907 @default.
• W2901848907 citedByCount "0" @default.
• W2901848907 crossrefType "journal-article" @default.
• W2901848907 hasAuthorship W2901848907A5006204901 @default.
• W2901848907 hasAuthorship W2901848907A5007579766 @default.
• W2901848907 hasAuthorship W2901848907A5023102915 @default.
• W2901848907 hasAuthorship W2901848907A5061337633 @default.
• W2901848907 hasAuthorship W2901848907A5063018006 @default.
• W2901848907 hasAuthorship W2901848907A5068290128 @default.
• W2901848907 hasAuthorship W2901848907A5088089771 @default.
• W2901848907 hasAuthorship W2901848907A5091712727 @default.
• W2901848907 hasConcept C11960822 @default.
• W2901848907 hasConcept C170493617 @default.
• W2901848907 hasConcept C178790620 @default.
• W2901848907 hasConcept C185592680 @default.
• W2901848907 hasConcept C195794163 @default.
• W2901848907 hasConcept C202751555 @default.
• W2901848907 hasConcept C2777411675 @default.
• W2901848907 hasConcept C2777622882 @default.
• W2901848907 hasConcept C2778326061 @default.
• W2901848907 hasConcept C519581460 @default.
• W2901848907 hasConcept C55493867 @default.
• W2901848907 hasConcept C86803240 @default.
• W2901848907 hasConcept C88045685 @default.
• W2901848907 hasConcept C95444343 @default.
• W2901848907 hasConceptScore W2901848907C11960822 @default.
• W2901848907 hasConceptScore W2901848907C170493617 @default.
• W2901848907 hasConceptScore W2901848907C178790620 @default.
• W2901848907 hasConceptScore W2901848907C185592680 @default.
• W2901848907 hasConceptScore W2901848907C195794163 @default.
• W2901848907 hasConceptScore W2901848907C202751555 @default.
• W2901848907 hasConceptScore W2901848907C2777411675 @default.
• W2901848907 hasConceptScore W2901848907C2777622882 @default.
• W2901848907 hasConceptScore W2901848907C2778326061 @default.
• W2901848907 hasConceptScore W2901848907C519581460 @default.
• W2901848907 hasConceptScore W2901848907C55493867 @default.
• W2901848907 hasConceptScore W2901848907C86803240 @default.
• W2901848907 hasConceptScore W2901848907C88045685 @default.
• W2901848907 hasConceptScore W2901848907C95444343 @default.
• W2901848907 hasFunder F4320337447 @default.
• W2901848907 hasIssue "S1" @default.
• W2901848907 hasLocation W29018489071 @default.
• W2901848907 hasOpenAccess W2901848907 @default.
• W2901848907 hasPrimaryLocation W29018489071 @default.
• W2901848907 hasRelatedWork W2004642028 @default.
• W2901848907 hasRelatedWork W2077267085 @default.
• W2901848907 hasRelatedWork W2089135366 @default.
• W2901848907 hasRelatedWork W2097392927 @default.
• W2901848907 hasRelatedWork W2166666983 @default.
• W2901848907 hasRelatedWork W2358248873 @default.
• W2901848907 hasRelatedWork W2363001730 @default.
• W2901848907 hasRelatedWork W2377870889 @default.
• W2901848907 hasRelatedWork W2384302969 @default.
• W2901848907 hasRelatedWork W2389251333 @default.
• W2901848907 hasVolume "32" @default.
• W2901848907 isParatext "false" @default.
• W2901848907 isRetracted "false" @default.
• W2901848907 magId "2901848907" @default.
• W2901848907 workType "article" @default.