scholarly journals Protein Expression in Vascular Endothelial Cells Obtained from Human Peripheral Arteries and Veins

2010 ◽  
Vol 47 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Annemarie E. Silver ◽  
Demetra D. Christou ◽  
Anthony J. Donato ◽  
Stacy D. Beske ◽  
Kerrie L. Moreau ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Peripheral Arteries ◽  
Arteries And Veins

scholarly journals Impact of Spaceflight and Artificial Gravity on the Mouse Retina: Biochemical and Proteomic Analysis

2018 ◽  
Vol 19 (9) ◽  
pp. 2546 ◽  
Author(s):  
Xiao Mao ◽  
Stephanie Byrum ◽  
Nina Nishiyama ◽  
Michael Pecaut ◽  
Vijayalakshmi Sridharan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Visual Acuity ◽  
Protein Expression ◽  
Proteomic Analysis ◽  
Vascular Endothelial Cells ◽  
Expression Profiles ◽  
Artificial Gravity ◽  
Ocular Tissue ◽  
Mouse Retina ◽  
Vascular Endothelial

Astronauts are reported to have experienced some impairment in visual acuity during their mission on the International Space Station (ISS) and after they returned to Earth. There is emerging evidence that changes in vision may involve alterations in ocular structure and function. To investigate possible mechanisms, changes in protein expression profiles and oxidative stress-associated apoptosis were examined in mouse ocular tissue after spaceflight. Nine-week-old male C57BL/6 mice (n = 12) were launched from the Kennedy Space Center on a SpaceX rocket to the ISS for a 35-day mission. The animals were housed in the mouse Habitat Cage Unit (HCU) in the Japan Aerospace Exploration Agency (JAXA) “Kibo” facility on the ISS. The flight mice lived either under an ambient microgravity condition (µg) or in a centrifugal habitat unit that produced 1 g artificial gravity (µg + 1 g). Habitat control (HC) and vivarium control mice lived on Earth in HCUs or normal vivarium cages, respectively. Quantitative assessment of ocular tissue demonstrated that the µg group induced significant apoptosis in the retina vascular endothelial cells compared to all other groups (p < 0.05) that was 64% greater than that in the HC group. Proteomic analysis showed that many key pathways responsible for cell death, cell repair, inflammation, and metabolic stress were significantly altered in µg mice compared to HC animals. Additionally, there were more significant changes in regulated protein expression in the µg group relative to that in the µg + 1 g group. These data provide evidence that spaceflight induces retinal apoptosis of vascular endothelial cells and changes in retinal protein expression related to cellular structure, immune response and metabolic function, and that artificial gravity (AG) provides some protection against these changes. These retinal cellular responses may affect blood–retinal barrier (BRB) integrity, visual acuity, and impact the potential risk of developing late retinal degeneration.

scholarly journals Low Shear Stress Upregulates CX3CR1 Expression by Inducing VCAM-1 via the NF-κB Pathway in Vascular Endothelial Cells

2020 ◽  
Vol 78 (3) ◽  
pp. 383-389 ◽  
Author(s):  
Yiwei Zhao ◽  
Peile Ren ◽  
Qiufang Li ◽  
Shafiu Adam Umar ◽  
Tan Yang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Critical Role ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Low Shear Stress ◽  
Low Shear ◽  
Cx3cr1 Expression

Abstract Atherosclerosis is a significant cause of mortality and morbidity. Studies suggest that the chemokine receptor CX3CR1 plays a critical role in atherogenesis. Shear stress is an important mechanical force that affects blood vessel function. In this study, we investigated the effect of shear stress on CX3CR1 expression in vascular endothelial cells (VECs). First, cells were exposed to different shear stress and then CX3CR1 mRNA and protein were measured by quantitative RT-PCR and western blot analysis, respectively. CX3CR1 gene silencing was used to analyze the molecular mechanisms underlying shear stress-mediated effects on CX3CR1 expression. CX3CR1 mRNA and protein expression were significantly increased with 4.14 dyne/cm2 of shear stress compared with other tested levels of shear stress. We observed a significant increase in CX3CR1 mRNA levels at 2 h and CX3CR1 protein expression at 4 h. CX3CR1-induced VCAM-1 expression in response to low shear stress by activating NF-κB signaling pathway in VECs. Our findings demonstrate that low shear stress increases CX3CR1 expression, which increases VCAM-1 expression due to elevated NF-κB activation. The current study provides evidence of the correlation between shear stress and atherosclerosis mediated by CX3CR1.

scholarly journals Effects of Simulated Microgravity on Ultrastructure and Apoptosis of Choroidal Vascular Endothelial Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Hongwei Zhao ◽  
Yuanyuan Shi ◽  
Changyu Qiu ◽  
Jun Zhao ◽  
Yubo Gong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cytochrome C ◽  
Protein Expression ◽  
Simulated Microgravity ◽  
Vascular Endothelial Cells ◽  
Chromatin Condensation ◽  
Microgravity Condition ◽  
Vascular Endothelial ◽  
Apoptosis Pathway ◽  
Mrna And Protein Expression

BackgroundIt was confirmed that simulated microgravity (SMG) led to ultrastructural alterations and apoptosis in many types of microvascular endothelial cells. However, whether SMG would also affect choroidal vascular endothelial cells (CVECs) remains unknown. This study was designed to investigate the effects of SMG on ultrastructure and apoptosis of CVECs.MethodsThe rotary cell culture system (RCCS) was utilized to simulate microgravity condition. Human CVECs were cultured under normal gravity (NG) or SMG condition for 3 days. The ultrastructure was viewed under transmission electron microscopy, and the organization of F-actin was observed by immunofluorescence staining. Additionally, the apoptosis percentage was calculated using flow cytometry. Moreover, the mRNA and protein expression of BAX, Bcl-2, Caspase3, Cytochrome C, p-AKT, and p-PI3K were detected with quantitative PCR and Western blot at different exposure time.ResultsIn the SMG group, CVECs presented with a shrunk cell body, chromatin condensation and margination, mitochondria vacuolization, and apoptotic bodies. The amount of F-actin decreased, and the filaments of F-actin were sparse or even partly discontinuous after cultivation under SMG for 72 h. The proportions of apoptotic CVECs in SMG groups at 24 and 72 h were significantly higher than those in the NG group (P &lt; 0.001). The mRNA and protein expression of Bax, Caspase3, and Cytochrome C of CVECs in SMG groups at 24 and 72 h significantly increased than those of the NG group, respectively (P &lt; 0.001). The alterations of p-AKT and p-PI3K protein expression possessed similar trends. On the contrary, the mRNA and protein expression of Bcl-2 in CVECs under SMG at 24 and 72 h were significantly less than that of the NG group, respectively (P &lt; 0.001).ConclusionSimulated microgravity conditions can lead the alterations of the F-actin structure and apoptosis of CVECs. The Bcl-2 apoptosis pathway and PI3K/AKT pathway may participate in the damage of CVECs caused by SMG.

scholarly journals Effects of IL-1β and TNF-α on the Expression of P311 in Vascular Endothelial Cells and Wound Healing in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Daijun Zhou ◽  
Tengfei Liu ◽  
Song Wang ◽  
Weifeng He ◽  
Wei Qian ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Control Group ◽  
Vascular Endothelial ◽  
Expression Levels ◽  
Relative Expression ◽  
Tnf Α

ObjectiveThis study aimed to define the role of interleukine-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the expression of P311 in vascular endothelial cells (VECs) and in wound healing.MethodsDAPI staining, a CCK-8 assay, cell migration assay, and an angiogenesis assay were used to assess the effects exerted by TNF-α and IL-1β at various concentrations on morphology, proliferation, migration, and angiogenesis of VECs. Western blot (WB) and reverse transcription-polymerase chain reaction (RT-PCR) models were employed to observe the effects exerted by proteins related to the nuclear factor-kappa B (NF-κB) signaling pathway and P311 mRNA expression. Bioinformatics analysis was performed on the binding sites of P311 and NF-κB. Finally, to investigate the effects of IL-1β and TNF-α on wound healing and the length of new epithelium in mice, we established a full-thickness wound defect model in mice. Immunohistochemistry was used to measure changes in P311, proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), CD31 (platelet endothelial cell adhesion molecule-1, PECAM-1/CD31), as well as other related proteins.ResultsWhen levels of TNF-α and IL-1β were both 20 ng/ml, their effects on cell proliferation, cytoskeleton protein expression, cell migration, and angiogenesis were the greatest (P &lt; 0.05). IL-1β and TNF-α at moderate concentrations effectively promoted P311 mRNA and p-NF-κB protein expression (P &lt; 0.05), while p-NF-K b protein expression was decreased (P &lt; 0.05). Luciferase assays showed that P311 expression was also relatively greater when stimulated at moderate concentrations (P &lt; 0.05), while relative expression was significantly lower when the p-NF-K b inhibitor CAPE was added (P &lt; 0.05). On 7-day wound healing rate comparison, the control, IL-1β, IL-1βab, TNF-α, and TNF-αab groups were 18, 37, 35, 39, and 36%, respectively, while control group + P311 siRNA was 31% (P &lt; 0.05). New epithelial length, granulation tissue thickness, and number of blood vessels trends were also the same. In the control group, P311 showed lower relative expression levels than the others (P &lt; 0.05). P311 relative expression levels trended as follows: control group &gt; IL-1βab &gt; IL-1β &gt; TNF-αab &gt; TNF-α (P &lt; 0.05).ConclusionWhen IL-1β and TNF-α concentrations are moderate, they effectively promote the proliferation, expression, migration, and angiogenesis of VECs, possibly by promoting the expression of the NF-K b pathway and thereby promoting the expression of P311. In vitro experiments on mice suggest that P311 effectively promotes wound healing, and its mechanism may be closely related to PCNA, CD31, and VEGF.

scholarly journals Reduction of GTP Cyclohydrolase I Feedback Regulating Protein Expression by Hydrogen Peroxide in Vascular Endothelial Cells

2005 ◽  
Vol 97 (2) ◽  
pp. 299-302 ◽  
Author(s):  
Masakazu Ishii ◽  
Shunichi Shimizu ◽  
Teruaki Wajima ◽  
Tamio Hagiwara ◽  
Takaharu Negoro ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Endothelial Cells ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Gtp Cyclohydrolase I ◽  
Gtp Cyclohydrolase

scholarly journals Leptin Induces C-Reactive Protein Expression in Vascular Endothelial Cells

2007 ◽  
Vol 27 (9) ◽  
Author(s):  
Prachi Singh ◽  
Michal Hoffmann ◽  
Robert Wolk ◽  
Abu S.M. Shamsuzzaman ◽  
Virend K. Somers
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Histamine reduces ZO-1 tight-junction protein expression in cultured retinal microvascular endothelial cells

1996 ◽  
Vol 320 (3) ◽  
pp. 717-721 ◽  
Author(s):  
Thomas W. GARDNER ◽  
Treena LESHER ◽  
Sonny KHIN ◽  
Cuong VU ◽  
Alistair J. BARBER ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Tight Junction ◽  
Protein Content ◽  
Vascular Endothelial Cells ◽  
Tight Junction Protein ◽  
Vascular Endothelial ◽  
Tight Junction Protein Expression ◽  
Junction Protein ◽  
Protein Alterations

We examined ZO-1 protein content in cultured retinal vascular endothelial cells to test the hypothesis that histamine alters tight-junction-protein expression. Histamine (10-9 –10-4 M) causes a reversible concentration-dependent reduction of ZO-1 protein content, mediated by both H1 and H2 receptors. Histamine reduces ZO-1 expression within the time associated with increased paracellular permeability. Tight-junction-protein alterations may be a novel explanation for the mechanism by which vasoactive agents increase microvascular permeability.

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