Simulated Microgravity Affects the TNF-α-Induced Interleukin Profile of Endothelial Cells Depending on the Initial ICAM-1 Expression

2021 ◽  
Vol 34 (1) ◽  
Author(s):  
E. G. Rudimov ◽  
Y. V. Rudimova ◽  
E. R. Andreeva ◽  
L. B. Buravkova
Keyword(s):  
Endothelial Cells ◽  
Simulated Microgravity ◽  
Tnf Α

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells

2020 ◽  
Vol 90 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Michael J. Haas ◽  
Marilu Jurado-Flores ◽  
Ramadan Hammoud ◽  
Victoria Feng ◽  
Krista Gonzales ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Coronary Artery ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Culture Media ◽  
Cytokine Secretion ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract. Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.5 mM dextrose for 24-hours and interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF α) levels were measured by enzyme immunoassays. To determine the effect of antioxidants on inflammatory cytokine secretion, cells were also treated with α-tocopherol, ascorbic acid, and the glutathione peroxidase mimetic ebselen. Only the concentration of IL-1β in culture media from cells exposed to 27.5 mM dextrose increased relative to cells maintained in 5.5 mM dextrose. Treatment with α-tocopherol (10, 100, and 1,000 μM) and ascorbic acid (15, 150, and 1,500 μM) at the same time that the dextrose was added reduced IL-1β, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1β, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. However, ebselen treatment reduced IL-1β, IL-6, and IL-8 levels in cells maintained in either 5.5 or 27.5 mM dextrose. IL-2 and TNF α concentrations in culture media were below the limit of detection under all experimental conditions studied suggesting that these cells may not synthesize detectable quantities of these cytokines. These results suggest that dextrose at certain concentrations may increase IL-1β levels and that antioxidants have differential effects on suppressing the secretion of pro-inflammatory cytokines in HCAEC.

scholarly journals Anti-Inflammatory Effect and Cellular Uptake Mechanism of Carbon Nanodots in in Human Microvascular Endothelial Cells

Nanomaterials ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1247
Author(s):  
Sarah Belperain ◽  
Zi Yae Kang ◽  
Andrew Dunphy ◽  
Brandon Priebe ◽  
Norman H. L. Chiu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Interleukin 1 ◽  
Antioxidant Properties ◽  
Synthesis Method ◽  
Microvascular Endothelial Cells ◽  
Carbon Nanodots ◽  
Uptake Mechanism ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Microvascular Endothelial

Cardiovascular disease (CVD) has become an increasingly important topic in the field of medical research due to the steadily increasing rates of mortality caused by this disease. With recent advancements in nanotechnology, a push for new, novel treatments for CVD utilizing these new materials has begun. Carbon Nanodots (CNDs), are a new form of nanoparticles that have been coveted due to the green synthesis method, biocompatibility, fluorescent capabilities and potential anti-antioxidant properties. With much research pouring into CNDs being used as bioimaging and drug delivery tools, few studies have been completed on their anti-inflammatory potential, especially in the cardiovascular system. CVD begins initially by endothelial cell inflammation. The cause of this inflammation can come from many sources; one being tumor necrosis factor (TNF-α), which can not only trigger inflammation but prolong its existence by causing a storm of pro-inflammatory cytokines. This study investigated the ability of CNDs to attenuate TNF-α induced inflammation in human microvascular endothelial cells (HMEC-1). Results show that CNDs at non-cytotoxic concentrations reduce the expression of pro-inflammatory genes, mainly Interleukin-8 (IL-8), and interleukin 1 beta (IL-1β). The uptake of CNDs by HMEC-1s was examined. Results from the studies involving channel blockers and endocytosis disruptors suggest that uptake takes place by endocytosis. These findings provide insights on the interaction CNDs and endothelial cells undergoing TNF-α induced cellular inflammation.

TNF-α decreases expression of Thrombomudulin and endothelial protein C receptor in human endothelial cells

2004 ◽  
Vol 121 (2) ◽  
pp. 290
Author(s):  
B. Nan ◽  
S. Yan ◽  
H. Chai ◽  
P. Lin ◽  
Q. Yao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein C ◽  
Endothelial Protein C Receptor ◽  
Human Endothelial Cells ◽  
Tnf Α

scholarly journals Posttranslational Modification of Bcl-2 Facilitates Its Proteasome-Dependent Degradation: Molecular Characterization of the Involved Signaling Pathway

2000 ◽  
Vol 20 (5) ◽  
pp. 1886-1896 ◽  
Author(s):  
Kristin Breitschopf ◽  
Judith Haendeler ◽  
Philipp Malchow ◽  
Andreas M. Zeiher ◽  
Stefanie Dimmeler
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Map Kinase ◽  
Specific Inhibitor ◽  
26S Proteasome ◽  
Apoptotic Pathway ◽  
Critical Determinant ◽  
Intact Cells ◽  
Antiapoptotic Protein ◽  
Tnf Α

ABSTRACT The ratio of proapoptotic versus antiapoptotic Bcl-2 members is a critical determinant that plays a significant role in altering susceptibility to apoptosis. Therefore, a reduction of antiapoptotic protein levels in response to proximal signal transduction events may switch on the apoptotic pathway. In endothelial cells, tumor necrosis factor alpha (TNF-α) induces dephosphorylation and subsequent ubiquitin-dependent degradation of the antiapoptotic protein Bcl-2. Here, we investigate the role of different putative phosphorylation sites to facilitate Bcl-2 degradation. Mutation of the consensus protein kinase B/Akt site or of potential protein kinase C or cyclic AMP-dependent protein kinase sites does not affect Bcl-2 stability. In contrast, inactivation of the three consensus mitogen-activated protein (MAP) kinase sites leads to a Bcl-2 protein that is ubiquitinated and subsequently degraded by the 26S proteasome. Inactivation of these sites within Bcl-2 revealed that dephosphorylation of Ser87 appears to play a major role. A Ser-to-Ala substitution at this position results in 50% degradation, whereas replacement of Thr74 with Ala leads to 25% degradation, as assessed by pulse-chase studies. We further demonstrated that incubation with TNF-α induces dephosphorylation of Ser87 of Bcl-2 in intact cells. Furthermore, MAP kinase triggers phosphorylation of Bcl-2, whereas a reduction in Bcl-2 phosphorylation was observed in the presence of MAP kinase-specific phosphatases or the MAP kinase-specific inhibitor PD98059. Moreover, we show that oxidative stress mediates TNF-α-stimulated proteolytic degradation of Bcl-2 by reducing MAP kinase activity. Taken together, these results demonstrate a direct protective role for Bcl-2 phosphorylation by MAP kinase against apoptotic challenges to endothelial cells and other cells.

Expression of P-selectin on Endothelial Cells is Upregulated by LPS and TNF-α in Vivo

1994 ◽  
Vol 2 (1) ◽  
pp. 7-14 ◽  
Author(s):  
Ursula Gotsch ◽  
Ute Jäger ◽  
Mara Dominis ◽  
Dietmar Vestweber
Keyword(s):  
Endothelial Cells ◽  
Tnf Α

scholarly journals Porphyromonas gingivalis Differentially Modulates Cell Death Profile in Ox-LDL and TNF-α Pre-Treated Endothelial Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0154590 ◽  
Author(s):  
Isaac Maximiliano Bugueno ◽  
Yacine Khelif ◽  
Narendra Seelam ◽  
David-Nicolas Morand ◽  
Henri Tenenbaum ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Porphyromonas Gingivalis ◽  
Tnf Α

ANISODAMINE ATTENTUATED TNF-α MEDIATED APOPTOSIS IN ENDOTHELIAL CELLS THROUGH A NF-A B-DEPENDENT MECHANISM

Shock ◽  
1999 ◽  
Vol 11 (Supplement) ◽  
pp. 19
Author(s):  
Lin Zhong ◽  
Weimin Xiao ◽  
Meidong Lui ◽  
Jialu You ◽  
Zhengyao Luo
Keyword(s):  
Endothelial Cells ◽  
Tnf Α ◽  
Dependent Mechanism
Sign in / Sign up

Export Citation Format

Share Document