scholarly journals Central Role of Metabolism in Endothelial Cell Function and Vascular Disease

Physiology ◽  
2017 ◽  
Vol 32 (2) ◽  
pp. 126-140 ◽  
Author(s):  
Laura Bierhansl ◽  
Lena-Christin Conradi ◽  
Lucas Treps ◽  
Mieke Dewerchin ◽  
Peter Carmeliet
Keyword(s):  
Endothelial Cell ◽  
Vascular Disease ◽  
Cell Function ◽  
Current Knowledge ◽  
Vascular Diseases ◽  
Vascular Endothelial ◽  
Endothelial Cell Function ◽  
Vascular Beds

The importance of endothelial cell (EC) metabolism and its regulatory role in the angiogenic behavior of ECs during vessel formation and in the function of different EC subtypes determined by different vascular beds has been recognized only in the last few years. Even more importantly, apart from a role of nitric oxide and reactive oxygen species in EC dysfunction, deregulations of EC metabolism in disease only recently received increasing attention. Although comprehensive metabolic characterization of ECs still needs further investigation, the concept of targeting EC metabolism to treat vascular disease is emerging. In this overview, we summarize EC-specific metabolic pathways, describe the current knowledge on their deregulation in vascular diseases, and give an outlook on how vascular endothelial metabolism can serve as a target to normalize deregulated endothelium.

Enhanced Vascular Endothelial Cell Function on Nanostructured Titanium Surface Features: The Role of Nano to Submicron Roughness

2008 ◽  
Vol 1136 ◽  
Author(s):  
Jing Lu ◽  
Dongwoo Khang ◽  
Thomas J. Webster
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Cell Function ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Function ◽  
Titanium Surfaces ◽  
Endothelial Cell Adhesion

ABSTRACTTo study the contribution of different surface feature properties in improving vascular endothelial cell adhesion, rationally designed nano/sub-micron patterns with various dimensions were created on titanium surfaces in this study. In vitro results indicated that endothelial cell adhesion was improved when the titanium pattern dimensions decreased into the nano-scale. Specifically, endothelial cells preferred to adhere on sub-micron and nano rough titanium substrates compared to flat titanium. Moreover, titanium with nano and sub-micron roughness and with the same chemistry as compared to flat titanium, had significantly greater surface energy. Thus, the present study indicated the strong potential of surface nanotopography and nano/sub-micron roughness for improving current vascular stent design.

Peroxynitrite increases iNOS through NF-κB and decreases prostacyclin synthase in endothelial cells

2002 ◽  
Vol 282 (2) ◽  
pp. C395-C402 ◽  
Author(s):  
Christy-Lynn M. Cooke ◽  
Sandra T. Davidge
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vascular Reactivity ◽  
Cell Function ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Cell Nuclei ◽  
Endothelial Cell Function ◽  
Protein Mass ◽  
Prostacyclin Synthase

Peroxynitrite, a marker of oxidative stress, is elevated in conditions associated with vascular endothelial cell dysfunction, such as atherosclerosis, preeclampsia, and diabetes. However, the effects of peroxynitrite on endothelial cell function are not clear. The endothelium-derived enzymes nitric oxide synthase (NOS) and prostaglandin H synthase (PGHS) mediate vascular reactivity and contain oxidant-sensitive isoforms (iNOS and PGHS-2) that can be induced by nuclear factor (NF)-κB activation. We investigated the effect(s) of peroxynitrite on NOS and PGHS pathways in endothelial cells. We hypothesized that peroxynitrite will increase levels of iNOS and PGHS-2 through activation of NF-κB. Western immunoblots of endothelial cells show that 3-morpholinosydnonimine (SIN-1; 0.5 mM), a peroxynitrite donor, increased iNOS protein mass, which can be inhibited by pyrroline dithiocarbamate (an NF-κB inhibitor) (167 ± 24.2 vs. 78 ± 19%, P < 0.05, n = 6). SIN-1 treatment also significantly increased NF-κB translocation into endothelial cell nuclei (135 ± 10%, P < 0.05). Endothelial NOS, PGHS-1, and PGHS-2 protein levels were not altered by SIN-1. However, prostacyclin synthase protein mass, but not mRNA, was significantly reduced in SIN-1-treated endothelial cells (78 ± 8.9%, P < 0.05). Our results illustrate novel mechanisms through which peroxynitrite may modulate vascular endothelial function.

Vitamin D Promotes Vascular Endothelial Cell Function via the Regulation of miR-199a-5p

2019 ◽  
Vol 9 (12) ◽  
pp. 1662-1669
Author(s):  
Lianman He ◽  
Yong Wang ◽  
Min Liu ◽  
Ling Li
Keyword(s):  
Vitamin D ◽  
Endothelial Cell ◽  
Cell Function ◽  
Vascular Endothelial Cell ◽  
Cell Counting ◽  
Biological Behavior ◽  
Luciferase Reporter ◽  
Vascular Endothelial ◽  
Endothelial Cell Function ◽  
The Impact

Essential hypertension (EH) is a main risk factor for cardiovascular disease. Vitamin D (VD) levels are inversely related to hypertension. MicroRNAs (miRNA or miR) are involved in various diseases, including EH. Till now, the role of miR-199a-5p in EH remains unclear. Cell counting kit-8, flow cytometry and Transwell assay were carried out in the current study to study the effects of VD on the biological behavior of Human umbilical vein endothelial cells (HUVECs). The expression of miR-199a-5p was subsequently determined using reverse transcription-quantitative (RT-q) PCR. TargetScan prediction and double luciferase reporter gene detection were applied to confirm the binding sites between Sirtuin 1 (SIRT1) and miR-199a-5p. The results showed that VD promoted the proliferation and migration of HUVECs and reduced cell apoptosis. VD was observed to significantly reduced miR-199a-5p level in HUVECs. Transfection of the miR-199a-5p mimic was indicated to reverse the influence of VD on the proliferation, migration and apoptosis of HUVECs. SIRT1 was also confirmed to be a target gene of miR-199a-5p. Western blot analysis and RT-qPCR were performed to measure the impact of VD on the SIRT1/AMP-activated protein kinase (AMPK)- /NFB pathway. The results demonstrated that VD increased SIRT1 expression and p-AMPK- and decreased the expression of p-p65, and the transfection of miR-199a-5p mimic reversed these effects. In conclusion, the results of the current study indicated that VD may relieve EH through promoting vascular endothelial cell function via regulating miR-199a-5p.

Deferoxamine promotes angiogenesis via the activation of vascular endothelial cell function

2011 ◽  
Vol 215 (2) ◽  
pp. 339-347 ◽  
Author(s):  
Yasumasa Ikeda ◽  
Soichiro Tajima ◽  
Sumiko Yoshida ◽  
Noriko Yamano ◽  
Yoshitaka Kihira ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Function ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Function

scholarly journals FKBPL and SIRT-1, key angiogenesis proteins, are downregulated by diabetes in pregnancy

2020 ◽  
Author(s):  
Abdelrahim Alqudah ◽  
Kelly-Ann Eastwood ◽  
Djurdja Jerotic ◽  
Naomi Todd ◽  
Denise Hoch ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protein Expression ◽  
Gestational Age ◽  
High Glucose ◽  
Cell Function ◽  
First Trimester ◽  
Diabetes In Pregnancy ◽  
Endothelial Cell Function ◽  
In Pregnancy

AbstractContextDiabetes in pregnancy is associated with numerous complications, however the mechanisms are still poorly understood.ObjectiveTo investigate the role of new angiogenesis markers, FKBPL and SIRT-1, in pre-gestational (type 1 diabetes, T1D) and gestational diabetes (GDM).Design and interventionPlacental FKBPL, SIRT-1, PlGF and VEGF-R1 protein expression was determined from pregnant women with GDM or T1D, and in first trimester trophoblast cells exposed to high glucose and varying oxygen concentrations. Endothelial cell function was assessed in high glucose conditions and FKBPL overexpression.Settings and ParticipantsHuman placental samples from pregnant women with GDM (n=6) or T1D (n=8) were collected to assess FKBPL and SIRT-1 protein expression compared to non-diabetic controls.Main outcome measuresTo determine the role of placental FKBPL and/or SIRT-1 in diabetic pregnancies, in first trimester trophoblasts and endothelial cell function in high-glucose environment.ResultsPlacental FKBPL protein expression was downregulated in T1D (FKBPL; p<0.05) whereas PlGF/VEGF-R1 were upregulated (p<0.05); correlations adjusted for gestational age were also significant. In the presence of GDM, only SIRT-1 (p<0.001) was significantly downregulated even when adjusted for gestational age (r=-0.92, p=0.001). FKBPL and SIRT-1 were also downregulated in ACH-3P cells in high glucose conditions and 6.5%/2.5% oxygen concentrations (p<0.05). FKBPL overexpression in HUVECs reduced tubule formation compared to empty vector control, in high glucose conditions (junctions; p<0.01, branches; p<0.05).ConclusionsFKBPL and/or SIRT-1 downregulation in response to diabetes may have a role in the development of vascular dysfunction in pregnancy, and associated complications such as preeclampsia.

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