scholarly journals Development of Small-Diameter Elastin-Silk Fibroin Vascular Grafts

2021 ◽  
Vol 8 ◽  
Author(s):  
Takashi Tanaka ◽  
Yasuyuki Abe ◽  
Chieh-Jen Cheng ◽  
Ryo Tanaka ◽  
Akira Naito ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Silk Fibroin ◽  
Vascular Endothelial Cells ◽  
Thrombus Formation ◽  
Vascular Grafts ◽  
Small Diameter ◽  
High Mobility ◽  
Water Soluble ◽  
Vascular Endothelial

Globally, increasing mortality from cardiovascular disease has become a problem in recent years. Vascular replacement has been used as a treatment for these diseases, but with blood vessels <6 mm in diameter, existing vascular grafts made of synthetic polymers can be occluded by thrombus formation or intimal hyperplasia. Therefore, the development of new artificial vascular grafts is desirable. In this study, we developed an elastin (EL)–silk fibroin (SF) double-raschel knitted vascular graft 1.5 mm in diameter. Water-soluble EL was prepared from insoluble EL by hydrolysis with oxalic acid. Compared to SF, EL was less likely to adhere to platelets, while vascular endothelial cells were three times more likely to adhere. SF artificial blood vessels densely packed with porous EL were fabricated, and these prevented the leakage of blood from the graft during implantation, while the migration of cells after implantation was promoted. Several kinds of 13C solid-state NMR spectra were observed with the EL–SF grafts in dry and hydrated states. It was noted that the EL molecules in the graft had very high mobility in the hydrated state. The EL–SF grafts were implanted into the abdominal aorta of rats to evaluate their patency and remodeling ability. No adverse reactions, such as bleeding at the time of implantation or disconnection of the sutured ends, were observed in the implanted grafts, and all were patent at the time of extraction. In addition, vascular endothelial cells were present on the graft's luminal surface 2 weeks after implantation. Therefore, we conclude that EL–SF artificial vascular grafts may be useful where small-diameter grafts are required.

Histidine-Rich Glycoprotein Inhibits High Mobility Group Box 1-Mediated Pathways in Vascular Endothelial Cells

2019 ◽  
Author(s):  
Shangze Gao ◽  
Hidenori Wake ◽  
Masakiyo Sakaguchi ◽  
Dengli Wang ◽  
Youhei Takahashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
High Mobility ◽  
High Mobility Group ◽  
Vascular Endothelial

scholarly journals NRP1 regulates HMGB1 in vascular endothelial cells under high homocysteine condition

2019 ◽  
Vol 316 (5) ◽  
pp. H1039-H1046 ◽  
Author(s):  
Yeshuo Ma ◽  
Zhen Zhang ◽  
Runtai Chen ◽  
Rui Shi ◽  
Pingyu Zeng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasma Level ◽  
Thoracic Aorta ◽  
Rat Model ◽  
Vascular Endothelial Cells ◽  
High Mobility ◽  
High Mobility Group ◽  
Vascular Endothelial ◽  
Endothelial Inflammation ◽  
Neuropilin 1

Endothelial inflammation plays an important role in hyperhomocysteinemia (HHcy)-associated vascular diseases. High mobility group box 1 (HMGB1) is a pro-inflammatory danger molecule produced by endothelial cells. However, whether HMGB1 is involved in vascular endothelial inflammation of HHcy is poorly understood. Neuropilin-1 (NRP1) mediates inflammatory response and activates mitogen-activated protein kinases (MAPKs) pathway that has been reported to be involved in regulation of HMGB1. The aim of this study was to determine the alteration of HMGB1 in HHcy, and the role of NRP1 in regulation of endothelial HMGB1 under high homocysteine (Hcy) condition. In the present study, we first observed that the plasma level of HMGB1 was elevated in HHcy patients and an experimental rat model, and increased HMGB1 was also observed in the thoracic aorta of an HHcy rat model. HMGB1 was induced by Hcy accompanied with upregulated NRP1 in vascular endothelial cells. Overexpression of NRP1 promoted expression and secretion of HMGB1 and endothelial inflammation; knockdown of NRP1 inhibited HMGB1 and endothelial inflammation induced by Hcy, which partially regulated through p38 MAPK pathway. Furthermore, NRP1 inhibitor ATWLPPR reduced plasma HMGB1 level and expression of HMGB1 in the thoracic aorta of HHcy rats. In conclusion, our data suggested that Hcy requires NRP1 to regulate expression and secretion of HMGB1. The present study provides the evidence for inhibition of NRP1 and HMGB1 to be the novel therapeutic targets of vascular endothelial inflammation in HHcy in the future. NEW & NOTEWORTHY This study shows for the first time to our knowledge that the plasma level of high mobility group box 1 (HMGB1) is elevated in hyperhomocysteinemia (HHcy) patients, and homocysteine promotes expression and secretion of HMGB1 partially regulated by neuropilin-1 in endothelial cells, which is involved in endothelial inflammation. Most importantly, these new findings will provide a potential therapeutic strategy for vascular endothelial inflammation in HHcy.

scholarly journals High-mobility group box 1 protein induces tissue factor expression in vascular endothelial cells via activation of NF-κB and Egr-1

2009 ◽  
Vol 102 (08) ◽  
pp. 352-359 ◽  
Author(s):  
Haichao Wang ◽  
Yiting Tang ◽  
Zhang Fan ◽  
Ben Lv ◽  
Xianzhong Xiao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Surface ◽  
Tissue Factor ◽  
Vascular Endothelial Cells ◽  
High Mobility ◽  
High Mobility Group ◽  
Cell Surface Receptors ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Surface Receptors

SummaryHigh-mobility group box 1 protein (HMGB1), an abundant nuclear protein, was recently established as a proinflammatory mediator of experimental sepsis.Although extracellular HMGB1 has been found in atherosclerotic plaques, its potential role in the pathogenesis of atherothrombosis remains elusive. In the present study, we determined whether HMGB1 induces tissue factor (TF) expression in vascular endothelial cells (ECs) and macrophages. Our data showed that HMGB1 stimulated ECs to express TF (but not TF pathway inhibitor) mRNA and protein in a concentration and time-dependent manner. Blockade of cell surface receptors (including TLR4, TLR2, and RAGE) with specific neutralising antibodies partially reduced HMGB1-induced TF expression. Moreover, HMGB1 increased expression of Egr-1 and nuclear translocation of NF-κB (c-Rel/p65) in ECs. Taken together, our data suggest that HMGB1 induces TF expression in vascular endothelial cells via cell surface receptors (TLR4, TLR2, and RAGE), and through activation of transcription factors (NF-κB and Egr-1).

scholarly journals TGF-β1 Potentiates the Cytotoxicity of Cadmium by Induction of a Metal Transporter, ZIP8, Mediated by the ALK5-Smad2/3 and ALK5-Smad3-p38 MAPK Signal Pathways in Cultured Vascular Endothelial Cells

2021 ◽  
Vol 23 (1) ◽  
pp. 448
Author(s):  
Keisuke Ito ◽  
Tomoya Fujie ◽  
Masahiro Shimomura ◽  
Tsuyoshi Nakano ◽  
Chika Yamamoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Transforming Growth Factor ◽  
Vascular Endothelial Cells ◽  
Extracellular Fluid ◽  
Mitogen Activated Protein Kinase ◽  
Signal Pathways ◽  
Vascular Endothelial ◽  
Metal Transporter ◽  
Tgf Β1

Vascular endothelial cells cover the luminal surface of blood vessels in a monolayer and play a role in the regulation of vascular functions, such as the blood coagulation-fibrinolytic system. When the monolayer is severely or repeatedly injured, platelets aggregate at the damaged site and release transforming growth factor (TGF)-β1 in large quantities from their α-granules. Cadmium is a heavy metal that is toxic to various organs, including the kidneys, bones, liver, and blood vessels. Our previous study showed that the expression level of Zrt/Irt-related protein 8 (ZIP8), a metal transporter that transports cadmium from the extracellular fluid into the cytosol, is a crucial factor in determining the sensitivity of vascular endothelial cells to cadmium cytotoxicity. In the present study, TGF-β1 was discovered to potentiate cadmium-induced cytotoxicity by increasing the intracellular accumulation of cadmium in cells. Additionally, TGF-β1 induced the expression of ZIP8 via the activin receptor-like kinase 5-Smad2/3 signaling pathways; Smad3-mediated induction of ZIP8 was associated with or without p38 mitogen-activated protein kinase (MAPK). These results suggest that the cytotoxicity of cadmium to vascular endothelial cells increases when damaged endothelial monolayers that are highly exposed to TGF-β1 are repaired.

scholarly journals Histidine-Rich Glycoprotein Inhibits High-Mobility Group Box-1-Mediated Pathways in Vascular Endothelial Cells through CLEC-1A

iScience ◽  
2020 ◽  
Vol 23 (6) ◽  
pp. 101180
Author(s):  
Shangze Gao ◽  
Hidenori Wake ◽  
Masakiyo Sakaguchi ◽  
Dengli Wang ◽  
Youhei Takahashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
High Mobility ◽  
High Mobility Group ◽  
Vascular Endothelial

Extracellular ATP signaling and P2X nucleotide receptors in monolayers of primary human vascular endothelial cells

2002 ◽  
Vol 282 (2) ◽  
pp. C289-C301 ◽  
Author(s):  
Lisa M. Schwiebert ◽  
William C. Rice ◽  
Brian A. Kudlow ◽  
Amanda L. Taylor ◽  
Erik M. Schwiebert
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Vessels ◽  
Vascular Tone ◽  
Vascular Endothelial Cells ◽  
Purinergic Signaling ◽  
Primary Cultures ◽  
Atp Release ◽  
Vascular Endothelial ◽  
Multiple Blood

ATP and its metabolites regulate vascular tone; however, the sources of the ATP released in vascular beds are ill defined. As such, we tested the hypothesis that all limbs of an extracellular purinergic signaling system are present in vascular endothelial cells: ATP release, ATP receptors, and ATP receptor-triggered signal transduction. Primary cultures of human endothelial cells derived from multiple blood vessels were grown as monolayers and studied using a bioluminescence detection assay for ATP released into the medium. ATP is released constitutively and exclusively across the apical membrane under basal conditions. Hypotonic challenge or the calcium agonists ionomycin and thapsigargin stimulate ATP release in a reversible and regulated manner. To assess expression of P2X purinergic receptor channel subtypes (P2XRs), we performed degenerate RT-PCR, sequencing of the degenerate P2XR product, and immunoblotting with P2XR subtype-specific antibodies. Results revealed that P2X4and P2X5are expressed abundantly by endothelial cell primary cultures derived from multiple blood vessels. Together, these results suggest that components of an autocrine purinergic signaling loop exist in the endothelial cell microvasculature that may allow for “self-regulation” of endothelial cell function and modulation of vascular tone.

scholarly journals Exogenous H2S Regulates of Cystathionine Gamma-Lyase in HUVECs During Hypoxia

2020 ◽  
Author(s):  
Maoxian Wang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Mrna Expression ◽  
Blood Vessels ◽  
Western Blotting ◽  
Promoter Activity ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Luciferase Assay ◽  
Vascular Endothelial

Cystathionine gamma-lyase (CSE) is one of the essential H2S-producing enzymes, and it regulates diverse functions in connection with cardiovascular function. It is crucial how exogenous H2S regulates CSE expression of the vascular endothelial cell during hypoxia. We examined the transcription and expression of CSE in HUVECs regulated by exogenous H2S with 100 μM during hypoxia by Luciferase assay, Western blotting, and quantitative RT-qPCR. Exogenous H2S influenced on the promoter activity of CSE in HUVECs during hypoxia. The effects of 100 μM H2S on CSE mRNA expression in HUVECs is decreased compared with 0 μM H2S. The consequences of 100 μM H2S on the expression level of CSE protein in HUVECs at two h of hypoxia is reduced compared with 0 μM H2S. These findings suggest that vascular endothelial cells can respond to the signals of hypoxia in the blood, and can respond to changes in H2S concentration in the blood, thus affect the blood vessels themselves.

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