scholarly journals Anti-inflammatory activity of Barleria lupulina: Identification of active compounds that activate the Nrf2 cell defense pathway, organize cortical actin, reduce stress fibers, and improve cell junctions in microvascular endothelial cells

2016 ◽  
Vol 193 ◽  
pp. 397-407 ◽  
Author(s):  
Donald R. Senger ◽  
Mien V. Hoang ◽  
Ki Hyun Kim ◽  
Chunshun Li ◽  
Shugeng Cao
Keyword(s):  
Endothelial Cells ◽  
Cell Junctions ◽  
Stress Fibers ◽  
Inflammatory Activity ◽  
Microvascular Endothelial Cells ◽  
Cortical Actin ◽  
Active Compounds ◽  
Cell Defense ◽  
Anti Inflammatory ◽  
Microvascular Endothelial

scholarly journals IL-8 activates endothelial cell CXCR1 and CXCR2 through Rho and Rac signaling pathways

2001 ◽  
Vol 280 (6) ◽  
pp. L1094-L1103 ◽  
Author(s):  
Ingrid U. Schraufstatter ◽  
Janice Chung ◽  
Meike Burger
Keyword(s):  
Endothelial Cells ◽  
Pertussis Toxin ◽  
Early Phase ◽  
Dominant Negative ◽  
Stress Fibers ◽  
Microvascular Endothelial Cells ◽  
Cortical Actin ◽  
Microvascular Endothelial ◽  
Cell Retraction ◽  
Later Phase

Stimulation of microvascular endothelial cells with interleukin (IL)-8 leads to cytoskeletal reorganization, which is mediated by combined activation of the CXCR1 and the CXCR2. In the early phase actin stress fibers appear, followed by cortical actin accumulation and cell retraction leading to gap formation between cells. The early response (between 1 and 5 min) is inhibited by an antibody that blocks the CXCR1. The later phase (from about 5 to 60 min), which is associated with cell retraction, is prevented by anti-CXCR2 antibody. Furthermore, anti-CXCR2, but not anti-CXCR1, antibody blocked IL-8-mediated haptotaxis of endothelial cells on collagen. The later phase of the IL-8-mediated actin response is inhibited by pertussis toxin, indicating that the CXCR2 couples to Gi. In contrast, the early phase is blocked by C3 botulinum toxin, which inactivates Rho, and by Y-27632, which inhibits Rho kinase, but not by pertussis toxin. Furthermore, the early CXCR1-mediated formation of stress fibers was prevented by dominant negative Rho. Dominant negative Rac on the other hand initially translocated to actin-rich filopodia after stimulation with IL-8 and later prevented cell retraction by blocking the CXCR2-mediated cytoskeletal response. These results indicate that IL-8 activates both the CXCR1 and the CXCR2 on microvascular endothelial cells, using different signal transduction cascades. The retraction of endothelial cells due to activation of the CXCR2 may contribute to the increased vascular permeability observed in acute inflammation and during the angiogenic response.

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.

Human Genome Screen to Identify the Genetic Basis of the Anti-inflammatory Effects ofBoswelliain Microvascular Endothelial Cells

2005 ◽  
Vol 24 (4) ◽  
pp. 244-255 ◽  
Author(s):  
Sashwati Roy ◽  
Savita Khanna ◽  
Hiral Shah ◽  
Cameron Rink ◽  
Christina Phillips ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Genome ◽  
Genetic Basis ◽  
Microvascular Endothelial Cells ◽  
Genome Screen ◽  
Anti Inflammatory ◽  
Microvascular Endothelial

scholarly journals Insulin and IGF1 receptors in human cardiac microvascular endothelial cells: metabolic, mitogenic and anti-inflammatory effects

2012 ◽  
Vol 215 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Karolina Bäck ◽  
Rakibul Islam ◽  
Git S Johansson ◽  
Simona I Chisalita ◽  
Hans J Arnqvist
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Inflammatory Responses ◽  
Receptor Protein ◽  
Microvascular Endothelial Cells ◽  
Tnf Α ◽  
Glucose Accumulation ◽  
Anti Inflammatory ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Diabetes is associated with microcirculatory dysfunction and heart failure and changes in insulin and IGF1 levels. Whether human cardiac microvascular endothelial cells (HMVEC-Cs) are sensitive to insulin and/or IGF1 is not known. We studied the role of insulin receptors (IRs) and IGF1 receptors (IGF1Rs) in metabolic, mitogenic and anti-inflammatory responses to insulin and IGF1 in HMVEC-Cs and human umbilical vein endothelial cells (HUVECs). IR and IGF1R gene expression was studied using real-time RT-PCR. Receptor protein expression and phosphorylation were determined by western blot and ELISA. Metabolic and mitogenic effects were measured as glucose accumulation and thymidine incorporation. An E-selectin ELISA was used to investigate inflammatory responses. According to gene expression and protein in HMVEC-Cs and HUVECs, IGF1R is more abundant than IR. Immunoprecipitation with anti-IGF1R antibody and immunoblotting with anti-IR antibody and vice versa, showed insulin/IGF1 hybrid receptors in HMVEC-Cs. IGF1 at a concentration of 10−8 mol/l significantly stimulated phosphorylation of both IGF1R and IR in HMVEC-Cs. In HUVECs IGF1 10−8 mol/l phosphorylated IGF1R. IGF1 stimulated DNA synthesis at 10−8 mol/l and glucose accumulation at 10−7 mol/l in HMVEC-Cs. TNF-α dramatically increased E-selectin expression, but no inflammatory or anti-inflammatory effects of insulin, IGF1 or high glucose were seen. We conclude that HMVEC-Cs express more IGF1Rs than IRs, and mainly react to IGF1 due to the predominance of IGF1Rs and insulin/IGF1 hybrid receptors. TNF-α has a pronounced pro-inflammatory effect in HMVEC-Cs, which is not counteracted by insulin or IGF1.

MKK3 and -6-dependent activation of p38α MAP kinase is required for cytoskeletal changes in pulmonary microvascular endothelial cells induced by ICAM-1 ligation

2005 ◽  
Vol 288 (2) ◽  
pp. L359-L369 ◽  
Author(s):  
Qin Wang ◽  
Michael Yerukhimovich ◽  
William A. Gaarde ◽  
Ian J. Popoff ◽  
Claire M. Doerschuk
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Map Kinase ◽  
Neutrophil Migration ◽  
P38 Map Kinase ◽  
Cell Junctions ◽  
Microvascular Endothelial Cells ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Neutrophil Adherence ◽  
Microvascular Endothelial

Previous studies demonstrated that neutrophil adherence induces ICAM-1-dependent cytoskeletal changes in TNF-α-treated pulmonary microvascular endothelial cells that are prevented by a pharmacological inhibitor of p38 MAP kinase. This study determined whether neutrophil adherence induces activation of p38 MAP kinase in endothelial cells, the subcellular localization of phosphorylated p38, which MAP kinase kinases lead to p38 activation, which p38 isoform is activated, and what the downstream targets may be. Confocal microscopy showed that neutrophil adhesion for 2 or 6 min induced an increase in phosphorylated p38 in endothelial cells that was punctate and concentrated in the central region of the endothelial cells. Studies using small interfering RNA (siRNA) to inhibit the protein expression of MAP kinase kinase 3 and 6, either singly or in combination, showed that both MAP kinase kinases were required for p38 phosphorylation. Studies using an antisense oligonucleotide to p38α demonstrated that inhibition of the protein expression of p38α 1) inhibited activation of p38 MAP kinase without affecting the protein expression of p38β; 2) prevented phosphorylation of heat shock protein 27, an actin binding protein that may induce actin polymerization upon phosphorylation; 3) attenuated cytoskeletal changes; and 4) attenuated neutrophil migration to the EC borders. Thus MAP kinase kinase3- and 6-dependent activation of the α-isoform of p38 MAP kinase is required for the cytoskeletal changes induced by neutrophil adherence and influences subsequent neutrophil migration toward endothelial cell junctions.

Erythromycin-induced CXCR4 expression on microvascular endothelial cells

2009 ◽  
Vol 297 (3) ◽  
pp. L420-L431 ◽  
Author(s):  
Yasuyuki Takagi ◽  
Naozumi Hashimoto ◽  
Sem H. Phan ◽  
Kazuyoshi Imaizumi ◽  
Masaki Matsuo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tissue Injury ◽  
Critical Role ◽  
Surface Expression ◽  
Membered Ring ◽  
Cxcr4 Expression ◽  
Microvascular Endothelial Cells ◽  
Anti Inflammatory ◽  
Microvascular Endothelial

Although stromal-derived factor-1 (SDF-1) via its cognate receptor CXCR4 is assumed to play a critical role in migration of endothelial cells during new vessel formation after tissue injury, CXCR4 expression on endothelial cells is strictly regulated. Erythromycin (EM), a 14-membered ring macrolide, has an anti-inflammatory effect that may account for its clinical benefit in the treatment of chronic inflammatory diseases. However, the effects of EM on endothelial cells and especially their expression of CXCR4 have not been fully evaluated. In this study, we demonstrated that EM markedly induced CXCR4 surface expression on microvascular endothelial cells in vitro and lung capillary endothelial cells in vivo. This ability to induce CXCR4 surface expression on endothelial cells was restricted to 14-membered ring macrolides and was not observed in other antibiotics including a 16-membered ring macrolide, josamycin. Furthermore, this EM-induced expression of CXCR4 on endothelial cells was functionally significant as demonstrated by chemotaxis assays in vitro. These findings suggest that EM-induced CXCR4 surface expression on endothelial cells may promote migration of CXCR4-expressing endothelial cells into sites of tissue injury, which may be associated with the known anti-inflammatory activity of this macrolide.

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