In vitro study of human vascular endothelial cell function on materials with various surface roughness

2004 ◽  
Vol 71A (1) ◽  
pp. 154-161 ◽  
Author(s):  
Chengyu Xu ◽  
Fang Yang ◽  
Shu Wang ◽  
Seeram Ramakrishna
Keyword(s):  
Surface Roughness ◽  
Endothelial Cell ◽  
Cell Function ◽  
Vascular Endothelial Cell ◽  
In Vitro Study ◽  
Vitro Study ◽  
Vascular Endothelial ◽  
Human Vascular Endothelial Cell ◽  
Endothelial Cell Function

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.

scholarly journals OR14-06 Inhibition of Protein Kinase C-beta2 Phosphorylation Restores Nuclear Factor-Kappa B Activation and Improves Peripheral Arterial Disease in Diabetes

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Satyanarayana Alleboina ◽  
Madhu V Singh ◽  
Thomas Wong ◽  
Ayotunde Dokun
Keyword(s):  
Endothelial Cell ◽  
High Glucose ◽  
Hind Limb ◽  
Prolonged Exposure ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Human Vascular Endothelial Cell ◽  
Normal Glucose ◽  
Akita Mice

Abstract Peripheral artery disease (PAD) is atherosclerotic occlusion of vessel outside the heart and most commonly affects the lower extremities. Diabetes (DM) accelerates the course and severity of PAD. Studies have shown that vascular endothelial cell NF-κB activity is required for post ischemic adaptation in experimental PAD. To better understand how DM contributes to PAD severity, we investigated the role of DM hyperglycemia in the activation of NF-κB under ischemic conditions. Induced ischemia in human vascular endothelial cell (HUVEC) cultures increased components of both canonical and non-canonical NF-κB pathways in the nucleus (p65 1.0 ± 0.1 vs 1.5 ± 0.2, p< 0.05, RelB 1.0 ± 0.1 vs 1.5 ± 0.2, p<0.01). Similarly, HUVEC acutely exposed to high glucose (HG, 25 mM) activated both canonical (IκB-α degradation, normal vs. HG 1.25 ± 0.02 vs 0.9 ± 0.0, p<0.05) and non-canonical NF-κB (p100 degradation, normal vs HG 0.021±0.001 vs 0.016±0.000, p<0.05) pathways. Prolonged exposure (3 days) of HUVEC to high glucose before ischemia resulted in impaired NF-κB activation as evident from decreased IκB phosphorylation (pIκB/IκB in normal glucose and ischemia 1.56 ± 0.22 vs 1.12 ± 0.35, p<0.01). To understand the signaling pathways underlying the ischemic activation of the NF-κB pathway, we used an array of antibodies to phosphoproteins involved in the inflammatory pathway. Compared to the lysates from cells grown in normal glucose, the lysates from cells grown in prolonged high glucose had dramatically increased phosphorylation of PKC-β2 (PKC-β2pSer661, 8-fold increase). To test whether this increase in PKC-β2pSer66 impairs NF-κB activation by ischemia, we treated HUVECS with prolonged high glucose exposure and ruboxystaurin (Rbx) (20 nM), an inhibitor of PKC-β2 phosphorylation, prior to ischemic exposure. Immunoblotting results confirmed that inhibition of PKC-β2 phosphorylation enhanced the ischemia induced NF-κB activation in HUVEC in this condition. We then tested the effect of Rbx on PKC-β2 phosphorylation and NF-κB activation in vivo in Akita mice, a model for type 1 diabetes. Consistent with our in vitro findings, in experimental PAD, NF-κB activity in the ischemic hind limb of Akita mice was significantly lower than those of the wild type (WT) mice as measured by IκB-α degradation (WT ischemic vs Akita ischemic; 0.04 ± 0.03 vs 0.10 ± 0.04 p<0.05). However, treatment of Akita mice with Rbx increased NF-κB activation in the ischemic hind limb (Akita ischemic 0.10 ± 0.04 vs ischemic+ Rbx 0.05 ± 0.02, p<0.05). Moreover, compared to the WT mice, the untreated Akita mice showed an impaired perfusion in the ischemic limbs (% perfusion recovery, WT vs Akita; 80.1 ± 10.3 vs 55.7 ± 10.1, p<0.05, n=5-8) that was improved in Rbx treated Akita mice (96.3 ± 2.3, p<0.01). Thus, hyperglycemic conditions increase PKC-β2pSer66 in endothelial cells attenuating salutary NF-κB activation contributing to poor PAD outcomes in DM.

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
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