scholarly journals Effects of Cinnamaldehyde on PGE2 Release and TRPV4 Expression in Mouse Cerebral Microvascular Endothelial Cells Induced by Interleukin-1β

2008 ◽  
Vol 31 (3) ◽  
pp. 426-430 ◽  
Author(s):  
Yue-Ying Ma ◽  
Hai-Ru Huo ◽  
Cang-Hai Li ◽  
Bao-Sheng Zhao ◽  
Lan-Fang Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Interleukin 1 ◽  
Microvascular Endothelial Cells ◽  
Interleukin 1 Beta ◽  
Microvascular Endothelial

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.

Induction of NO synthase in rat cardiac microvascular endothelial cells by IL-1 beta and IFN-gamma

1995 ◽  
Vol 268 (3) ◽  
pp. H1293-H1303 ◽  
Author(s):  
J. L. Balligand ◽  
D. Ungureanu-Longrois ◽  
W. W. Simmons ◽  
L. Kobzik ◽  
C. J. Lowenstein ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Interleukin 1 ◽  
No Synthase ◽  
Microvascular Endothelial Cells ◽  
Inos Mrna ◽  
Microvascular Endothelium ◽  
Ifn Gamma ◽  
Nitrite Production ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

There are important phenotypic differences between endothelial cells of large vessels and the microvasculature and among microvascular endothelial cells isolated from different tissues and organs. In contrast to most macrovascular endothelial cells, we demonstrate that cultured cardiac microvascular endothelial cells (CMEC) have no detectable constitutive NO synthase (NOS) activity but have a robust increase in NOS activity in response to specific inflammatory cytokines. To determine the identity of the inducible NOS (iNOS) isoform(s) induced by cytokines, we used reverse-transcription polymerase chain reaction techniques to clone and sequence a 217-bp cDNA fragment from CMEC cultures pretreated with interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) that was identical to the corresponding portion of the murine macrophage iNOS cDNA. By use of this CMEC iNOS cDNA as a probe in Northern analyses, IL-1 beta, but not IFN-gamma, increased iNOS mRNA content in CMEC, although IFN-gamma markedly potentiated iNOS induction in these cells. In IL-1 beta- and IFN-gamma-pretreated CMEC, dexamethasone only minimally suppressed the rise in iNOS mRNA, protein abundance, or maximal iNOS enzyme activity in whole cell lysates but suppressed nitrite production by 60% in intact CMEC. Dual labeling of cytokine-pretreated CMEC in primary culture with an anti-iNOS antiserum and a fluorescein-labeled lectin specific for the microvascular endothelium of rat heart (GS-1) confirmed the presence of iNOS expression in these cells. iNOS was also detected in microvascular endothelium in situ in ventricular muscle from lipopolysaccharide-, but not sham-injected, rat hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Noninflammatory Expression of E-Selectin Is Regulated by Cell Growth

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3785-3791
Author(s):  
Jianying Luo ◽  
Gretchen Paranya ◽  
Joyce Bischoff
Keyword(s):  
Endothelial Cells ◽  
Interleukin 1 ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Microvascular Endothelial Cells ◽  
Proliferating Cells ◽  
Microvascular Endothelial ◽  
In Cells

E-selectin, an endothelial-specific adhesion molecule best known for its role in leukocyte adhesion, is not detected in quiescent endothelial cells, but is induced by inflammatory stimuli. However, E-selectin is also expressed in proliferating endothelial cells under noninflammatory conditions in vivo and in vitro, suggesting that E-selectin is also regulated by growth signals. To investigate E-selectin expression in lipopolysaccharide-stimulated versus nonstimulated proliferating cells, we analyzed the distribution of E-selectin–positive human microvascular endothelial cells in G0/G1, S, and G2/M phases of the cell cycle under both conditions. Lipopolysaccharide treatment resulted in uniformly increased E-selectin expression in cells in G0/G1, S, and G2/M. In contrast, levels of E-selectin in nonstimulated proliferating cells showed a linear correlation with the percentage of cells in G2/M. E-selectin in proliferating endothelial cells was not reduced by addition of soluble tumor necrosis factor-–receptor or soluble interleukin-1–receptor indicating that its expression was not due to endogenous production of either cytokine. In addition, E-selectin was increased in cells stimulated with basic fibroblast growth factor, a well-known mitogen for endothelial cells. E-selectin in proliferating endothelial cells is functional, as shown by E-selectin–dependent adhesion of the promyelocytic leukemia cell line HL-60 to subconfluent human microvascular endothelial cells. In summary, these studies indicate that E-selectin can be regulated by a non-inflammatory pathway that is related to the proliferative state of the endothelium.

Noninflammatory Expression of E-Selectin Is Regulated by Cell Growth

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3785-3791 ◽  
Author(s):  
Jianying Luo ◽  
Gretchen Paranya ◽  
Joyce Bischoff
Keyword(s):  
Endothelial Cells ◽  
Interleukin 1 ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Microvascular Endothelial Cells ◽  
Proliferating Cells ◽  
Microvascular Endothelial ◽  
In Cells

Abstract E-selectin, an endothelial-specific adhesion molecule best known for its role in leukocyte adhesion, is not detected in quiescent endothelial cells, but is induced by inflammatory stimuli. However, E-selectin is also expressed in proliferating endothelial cells under noninflammatory conditions in vivo and in vitro, suggesting that E-selectin is also regulated by growth signals. To investigate E-selectin expression in lipopolysaccharide-stimulated versus nonstimulated proliferating cells, we analyzed the distribution of E-selectin–positive human microvascular endothelial cells in G0/G1, S, and G2/M phases of the cell cycle under both conditions. Lipopolysaccharide treatment resulted in uniformly increased E-selectin expression in cells in G0/G1, S, and G2/M. In contrast, levels of E-selectin in nonstimulated proliferating cells showed a linear correlation with the percentage of cells in G2/M. E-selectin in proliferating endothelial cells was not reduced by addition of soluble tumor necrosis factor-–receptor or soluble interleukin-1–receptor indicating that its expression was not due to endogenous production of either cytokine. In addition, E-selectin was increased in cells stimulated with basic fibroblast growth factor, a well-known mitogen for endothelial cells. E-selectin in proliferating endothelial cells is functional, as shown by E-selectin–dependent adhesion of the promyelocytic leukemia cell line HL-60 to subconfluent human microvascular endothelial cells. In summary, these studies indicate that E-selectin can be regulated by a non-inflammatory pathway that is related to the proliferative state of the endothelium.

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