Changes in copper concentrations affect the protein levels but not the mRNA levels of copper chaperones in human umbilical vein endothelial cells

Metallomics ◽  
2014 ◽  
Vol 6 (3) ◽  
pp. 554-559 ◽  
Author(s):  
Daoyin Dong ◽  
Xinhua Xu ◽  
Wen Yin ◽  
Y. James Kang
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Mrna Levels ◽  
Copper Chaperones ◽  
Human Umbilical Vein ◽  
Protein Levels ◽  
Umbilical Vein Endothelial Cells

Lysophosphatidylcholine Decreases the Synthesis of Tissue Factor Pathway Inhibitor in Human Umbilical Vein Endothelial Cells

1998 ◽  
Vol 79 (01) ◽  
pp. 217-221 ◽  
Author(s):  
Koichi Kokame ◽  
Toshiyuki Miyata ◽  
Naoaki Sato ◽  
Hisao Kato
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Umbilical Vein ◽  
Mrna Levels ◽  
Down Regulation ◽  
Human Umbilical Vein ◽  
Tissue Factor Pathway ◽  
Umbilical Vein Endothelial Cells

SummaryThrombotic complications are frequently associated with atherosclerosis. Lysophosphatidylcholine (LPC), a component accumulated in oxidatively modified LDL (ox-LDL), is known to play a crucial role in the initiation and progression of atherosclerotic vascular lesions. Since a vascular anticoagulant, tissue factor pathway inhibitor (TFPI), has the function of regulating the initial reaction of tissue factor (TF)-induced coagulation, we investigated the effect of LPC on TFPI synthesis in cultured human umbilical vein endothelial cells (HUVEC). The treatment of HUVEC with LPC for 24 h decreased TFPI antigen levels in both the culture medium and the cell lysate in a dose-dependent manner. Northern blot analysis revealed that LPC caused a time-dependent decrease in the TFPI mRNA levels. The levels of TFPI antigen and mRNA were decreased to 72% and 38%, respectively, by the incubation with 50 μM LPC for 24 h. The down-regulation by LPC of TFPI mRNA expression was not observed in the presence of cycloheximide, suggesting that protein synthesis was involved in the suppression of TFPI mRNA expression. The TFPI mRNA levels in actinomycin D-treated cells were relatively stable, indicating that the down-regulation of TFPI mRNA by LPC would be partly explained by the enhanced mRNA destabilization. In contrast to the significant down-regulatory effects of LPC on TFPI expression, LPC did not induce TF mRNA expression in HUVEC. These results indicate that LPC accumulated in the atherosclerotic vascular wall would suppress endothelial TFPI synthesis, reducing the antithrombotic property of endothelial cells.

scholarly journals Up-regulation of thrombomodulin by activation of histamine H1-receptors in human umbilical-vein endothelial cells in vitro

1991 ◽  
Vol 276 (3) ◽  
pp. 739-743 ◽  
Author(s):  
K Hirokawa ◽  
N Aoki
Keyword(s):  
Endothelial Cells ◽  
Phorbol Esters ◽  
Umbilical Vein ◽  
Feedback Regulation ◽  
Mrna Levels ◽  
Human Umbilical Vein ◽  
H2 Antagonist ◽  
Histamine H1 Receptors ◽  
Umbilical Vein Endothelial Cells

Previous reports demonstrated that the expression of thrombomodulin (TM) in endothelial cells was modulated by various agents. Although TM was down-regulated by endotoxin or cytokines, up-regulation of TM was accomplished when endothelial cells were stimulated with unphysiologically high concentrations of cyclic AMP derivatives or tumour-promoting phorbol esters. We investigated the expression of TM in human umbilical-vein endothelial cells (HUVECs) by physiological substances that can be released into the bloodstream. Histamine (0.1-10 microM, 1-48 h) increased TM activity, TM antigen in cell lysates and TM mRNA levels, but 5-hydroxytryptamine and bradykinin had no effect. Enhancement of TM activity by histamine was completely blocked by the H1-selective antagonist pyrilamine, whereas the H2-antagonist cimetidine had no effect, showing that histamine up-regulates TM activity via H1-receptors on HUVECs. Enhanced TM activity by histamine and the resultant increase in protein C activation might play a role in a feedback regulation for prevention of vascular thrombosis.

Transforming Growth Factor Betal and Beta2 Induce Down-Modulation of Thrombomodulin in Human Umbilical Vein Endothelial Cells

1995 ◽  
Vol 73 (05) ◽  
pp. 812-818 ◽  
Author(s):  
Taro Ohji ◽  
Hajime Urano ◽  
Akira Shirahata ◽  
Minoru Yamagishi ◽  
Ken Higashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Time Course ◽  
Transforming Growth Factor ◽  
Umbilical Vein ◽  
Mrna Levels ◽  
Antigen Level ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1

SummaryTo investigate the effects of transforming growth factor-betas (TGF-βs) on endothelial anticoagulant activity, we assayed thrombomodulin (TM) activity and antigen levels of human umbilical vein endothelial cells (HUVECs) incubated with TGF-βs in vitro. TGF-β1 suppressed surface TM activity and surface TM antigen levels maximally 12 h after incubation in dose-dependent manners. TGF-β2 was almost equipotent with TGF-β1 for the suppression of them. Both TGF-βs suppressed total TM antigen level in HUVECs, and the time course of the suppression was similar to that of the cell surface TM antigen level. The maximal reductions of TM mRNA levels by TGF-βs were observed at several hours ahead of those observed in both surface and total TM antigen levels, suggesting that the TGF-β-mediated suppression of TM antigen of HUVECs is primarily regulated at the TM mRNA level. Our present work suggests that the down-modulation of TM level induced by TGF-βs in HUVECs contributes in vivo to promoting the thrombogenesis either at the sites of injury of vessel walls, such as atherosclerotic lesions where TGF-β1 is released from platelets, smooth muscle cells and monocytes, or at neovascular walls in tumors secreting TGF-β2.

scholarly journals Evodiamine Attenuates P2X7-Mediated Inflammatory Injury of Human Umbilical Vein Endothelial Cells Exposed to High Free Fatty Acids

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yun Xue ◽  
Ting Guo ◽  
Lifang Zou ◽  
Yingxin Gong ◽  
Bing Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Endothelial Cells ◽  
Free Fatty Acids ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Umbilical Vein Endothelial Cells

Insulin resistance and type 2 diabetes mellitus (T2DM) are highly prevalent around the world. Elevated concentrations of free fatty acids (FFAs) are closely related to insulin resistance and T2DM. P2X7 receptor is an ion channel gated by ATP, which is implicated in various scenarios including immune response, pain, and inflammation. In this study, we have explored whether P2X7 receptor is involved in pathological changes in human umbilical vein endothelial cells (HUVECs) induced by high FFA treatment, and the potential beneficial effects of evodiamine. Evodiamine could effectively suppress the enhanced expression of P2X7 receptor caused by high FFAs at both mRNA and protein levels. In addition, high FFA-induced cytotoxicity, the upregulated release of ATP, and production of reactive oxygen species (ROS) could be ameliorated by evodiamine in HUVECs. Evodiamine could also reverse the decreased NO formation and the increased adhesive events of immune cells at high FFAs. Moreover, evodiamine inhibited P2X7-dependent TNF-α expression and ERK 1/2 phosphorylation due to high FFAs. All these results indicated that evodiamine could correct the upregulated expression of P2X7 receptor induced under high FFA condition in HUVECs, and consequently suppressed oxidative stress and inflammatory responses.

scholarly journals YB-1 transferred by gastric cancer exosomes promotes angiogenesis via enhancing the expression of angiogenic factors in vascular endothelial cells

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Xiaoxia Xue ◽  
Jin Huang ◽  
Kai Yu ◽  
Xinyue Chen ◽  
Yini He ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Angiogenic Factors ◽  
Mrna Levels ◽  
Protein Levels ◽  
Significant Difference ◽  
Umbilical Vein Endothelial Cells ◽  
Intercellular Communications

Abstract Background Angiogenesis is important for the progression of gastric cancer (GC). Y-box binding protein 1 (YB-1) predicts advanced disease and indicates neovasculature formation in GC tissues, while the related mechanisms remain elusive. Exosomes mediate intercellular communications via transferring various molecules including proteins, lipids, mRNAs, and microRNAs, while the cargos of GC exosomes and the related mechanisms in GC angiogenesis were rarely reported except for several microRNAs. Methods In this study, human umbilical vein endothelial cells (HUVECs) were, respectively, treated by the exosomes isolated from the YB-1 transfected and the control SGC-7901 cells (SGC-7901-OE-Exo and SGC-7901-NC-Exo), and their apoptosis, proliferation, migration, invasion, and angiogenesis were, sequentially, compared. The levels of angiogenic factors including VEGF, Ang-1, MMP-9 and IL-8 in the exosome-treated HUVECs and the GC-derived exosomes were, separately, detected using PCR and Western blotting as well as RNA sequencing assays. Results We observed the consistent level of YB-1 in the exosomes and their originated GC cells, and the internalization of exosomes into HUVECs. Comparing with SGC-7901-NC-Exo, SGC-7901-OE-Exo significantly inhibited the apoptosis but promoted the proliferation, migration, invasion, and angiogenesis of HUVECs, within which the increased mRNA and protein levels of VEGF, Ang-1, MMP-9 and IL-8 were demonstrated. Meanwhile, mRNA levels of VEGF, Ang-1, MMP-9 and IL-8 showed no significant difference between SGC-7901-NC-Exo and SGC-7901-OE-Exo, although statistically higher mRNA of YB-1 was detected in the SGC-7901-OE-Exo. Conclusions Our findings illustrate YB-1 as the key component of exosome to promote GC angiogenesis by upregulating specific angiogenic factors in the exosome-treated endothelial cells but not in the exosomes themselves.

scholarly journals Thrombin regulation of mRNA levels of tissue plasminogen activator and plasminogen activator inhibitor-1 in cultured human umbilical vein endothelial cells

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 222-228 ◽  
Author(s):  
D Dichek ◽  
T Quertermous
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Umbilical Vein ◽  
Plasminogen Activator Inhibitor ◽  
Mrna Levels ◽  
Human Umbilical Vein ◽  
Tissue Plasminogen ◽  
Umbilical Vein Endothelial Cells ◽  
Activator Inhibitor ◽  
Pai 1

Abstract Cultured human umbilical vein endothelial cells release tissue plasminogen activator (t-PA) and type 1 plasminogen activator inhibitor (PAI-1) in response to alpha thrombin stimulation. In order to study the mechanisms of thrombin stimulation, we measured changes in levels of mRNA for t-PA and PAI-1 following exposure of endothelial cells to 3 U/mL alpha thrombin. Alpha thrombin causes a significant and time- dependent increase in the mRNA levels of both t-PA and PAI-1. Catalytically inactivated diisofluorophosphate (DIP) treated thrombin and alpha thrombin pretreated with hirudin do not alter t-PA and PAI-1 mRNA levels. We conclude that the increased secretion of t-PA and PAI-1 by human umbilical vein endothelial cells in response to alpha thrombin is mediated at least partially through an increase in mRNA levels. In addition, an active thrombin catalytic site is required for these increases in mRNA to occur.

scholarly journals Thrombin regulation of mRNA levels of tissue plasminogen activator and plasminogen activator inhibitor-1 in cultured human umbilical vein endothelial cells

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 222-228 ◽  
Author(s):  
D Dichek ◽  
T Quertermous
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Umbilical Vein ◽  
Plasminogen Activator Inhibitor ◽  
Mrna Levels ◽  
Human Umbilical Vein ◽  
Tissue Plasminogen ◽  
Umbilical Vein Endothelial Cells ◽  
Activator Inhibitor ◽  
Pai 1

Cultured human umbilical vein endothelial cells release tissue plasminogen activator (t-PA) and type 1 plasminogen activator inhibitor (PAI-1) in response to alpha thrombin stimulation. In order to study the mechanisms of thrombin stimulation, we measured changes in levels of mRNA for t-PA and PAI-1 following exposure of endothelial cells to 3 U/mL alpha thrombin. Alpha thrombin causes a significant and time- dependent increase in the mRNA levels of both t-PA and PAI-1. Catalytically inactivated diisofluorophosphate (DIP) treated thrombin and alpha thrombin pretreated with hirudin do not alter t-PA and PAI-1 mRNA levels. We conclude that the increased secretion of t-PA and PAI-1 by human umbilical vein endothelial cells in response to alpha thrombin is mediated at least partially through an increase in mRNA levels. In addition, an active thrombin catalytic site is required for these increases in mRNA to occur.

scholarly journals 17β-estradiol upregulates striatin protein levels via Akt pathway in human umbilical vein endothelial cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0202500 ◽  
Author(s):  
Shuhui Zheng ◽  
Peng Sun ◽  
Haimei Liu ◽  
Runmei Li ◽  
Lingli Long ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Akt Pathway ◽  
Human Umbilical Vein ◽  
Protein Levels ◽  
17Β Estradiol ◽  
Umbilical Vein Endothelial Cells

Sp1-mediated downregulation of P2X4 receptor gene transcription in endothelial cells exposed to shear stress

2001 ◽  
Vol 280 (5) ◽  
pp. H2214-H2221 ◽  
Author(s):  
Risa Korenaga ◽  
Kimiko Yamamoto ◽  
Norihiko Ohura ◽  
Takaaki Sokabe ◽  
Akira Kamiya ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Gene Transcription ◽  
Fluid Shear Stress ◽  
Adenine Nucleotides ◽  
Umbilical Vein ◽  
Receptor Gene ◽  
Mrna Levels ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Endothelial purinoceptors play an important role in vascular responses to extracellular adenine nucleotides and hemodynamic forces. Here we report that P2X4 purinoceptor expression in human umbilical vein endothelial cells is transcriptionally downregulated by fluid shear stress. When human umbilical vein endothelial cells were subjected to a laminar shear stress of 15 dyn/cm2, P2X4 mRNA levels began to decrease within 1 h and further decreased with time, reaching 60% at 24 h. Functional analysis of the 1.9-kb P2X4 5′-promoter indicated that a 131-bp segment (−112 to +19 bp relative to the transcription start site) containing a consensus binding site for the Sp1 transcription factor was critical for the shear stress responsiveness. Mutations of the Sp1 site decreased the basal level of transcription and abolished the response of the P2X4 promoter to shear stress. Electrophoretic mobility shift assays showed a marked decrease in binding of Sp1 to the Sp1 consensus element in shear-stressed cells, suggesting that Sp1 mediates the shear stress-induced downregulation of P2X4 gene transcription.

scholarly journals IRE1 Endoribonuclease Activity Modulates Hypoxic HIF-1α Signaling in Human Endothelial Cells

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 895 ◽  
Author(s):  
Adrianna Moszyńska ◽  
James F. Collawn ◽  
Rafal Bartoszewski
Keyword(s):  
Endothelial Cells ◽  
Target Genes ◽  
Umbilical Vein ◽  
Mrna Levels ◽  
Endonuclease Activity ◽  
Independent Manner ◽  
Protein Levels ◽  
The Unfolded Protein Response ◽  
Umbilical Vein Endothelial Cells ◽  
Sirna Knockdown

While the role of hypoxia and the induction of the hypoxia inducible factors (HIFs) and the unfolded protein response (UPR) pathways in the cancer microenvironment are well characterized, their roles and relationship in normal human endothelium are less clear. Here, we examined the effects of IRE1 on HIF-1α protein levels during hypoxia in primary human umbilical vein endothelial cells (HUVECs). The results demonstrated that HIF-1α levels peaked at 6 h of hypoxia along with two of their target genes, GLUT1 and VEGFA, whereas at up to 12 h of hypoxia the mRNA levels of markers of the UPR, IRE1, XBP1s, BiP, and CHOP, did not increase, suggesting that the UPR was not activated. Interestingly, the siRNA knockdown of IRE1 or inhibition of IRE1 endonuclease activity with 4µ8C during hypoxia significantly reduced HIF-1α protein without affecting HIF1A mRNA expression. The inhibition of the endonuclease activity with 4µ8C in two other primary endothelial cells during hypoxia, human cardiac microvascular endothelial cells and human aortic endothelial cells showed the same reduction in the HIF-1α protein. Surprisingly, the siRNA knockdown of XBP1s during hypoxia did not decrease the HIF1α protein levels, indicating that the IRE1-mediated effect on stabilizing the HIF1α protein levels was XBP1s-independent. The studies presented here, therefore, provide evidence that IRE1 activity during hypoxia increases the protein levels of HIF1α in an XBP1s-independent manner.

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