Interleukin-1 induces major phenotypic changes in human skin microvascular endothelial cells

1997 ◽  
Vol 173 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Luz I. Romero ◽  
Dan-Ning Zhang ◽  
G. Scott Herron ◽  
Marvin A. Karasek
Keyword(s):  
Endothelial Cells ◽  
Human Skin ◽  
Interleukin 1 ◽  
Microvascular Endothelial Cells ◽  
Phenotypic Changes ◽  
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)

scholarly journals Immunoelectron Microscopic Characterization of Human Dermal Lymphatic Microvascular Endothelial Cells: Differential Expression of CD31, CD34, and Type IV Collagen with Lymphatic Endothelial Cells vs Blood Capillary Endothelial Cells in Normal Human Skin, Lymphangioma, and Hemangioma In Situ

1998 ◽  
Vol 46 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Birthe Sauter ◽  
Dagmar Foedinger ◽  
Barbara Sterniczky ◽  
Klaus Wolff ◽  
Klemens Rappersberger
Keyword(s):  
Endothelial Cells ◽  
Human Skin ◽  
Type Iv Collagen ◽  
Microvascular Endothelial Cells ◽  
Lymphatic Endothelial Cells ◽  
Normal Human Skin ◽  
Type Iv ◽  
Normal Human ◽  
Microvascular Endothelial

We performed a comparative investigation of the immunomorphological characteristics of lymphatic and blood microvascular endothelial cells in normal human skin, cutaneous lymphangiomas, and hemangiomas, employing a pre-embedding immunogold electron microscopic technique. We stained for cell membrane proteins that are commonly used for light microscopic characterization of blood endothelial cells. With blood microvascular endothelial cells, we observed uniform labeling of the luminal cell membranes with monoclonal antibodies (MAbs) JC70 (CD31), EN-4 (CD31), BMA120, PAL-E, and QBEND-10 (CD34), and strong staining of the vascular basal lamina for Type IV collagen under normal and pathological conditions. In contrast, lymphatic microvascular endothelial cells in normal human skin and in lymphangiomas displayed, in addition to a luminal labeling, pronounced expression of CD31 and CD34 along the abluminal cell membranes. Moreover, CD31 was preferentially detected within intercellular junctions. The expression of CD34 was mostly confined to abluminal endothelial microprocesses and was upregulated in lymphangiomas and hemangiomas. Type IV collagen partially formed the luminal lining of initial lymphatics and occasionally formed bridges over interendothelial gaps. Our findings suggest a function of transmigration protein CD31 in recruitment of dendritic cells into the lymphatic vasculature. CD34 labeling may indicate early endothelial cell sprouting. The distribution of Type IV collagen also supports its role as a signal for migration and tube formation for lymphatic endothelial cells.

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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