Search results for: Human Large Intestine Microvascular Endothelial Cells
#30569099 // Save this To Up
Kaempferol inhibits multiple pathways involved in the secretion of inflammatory mediators from LPS‑induced rat intestinal microvascular endothelial cells.Inflammatory bowel disease (IBD) is a chronic, idiopathic inflammatory disease of the small and/or large intestine. Endothelial expression of inflammatory mediators, including cytokines and adhesion molecules, serves a critical role in the initiation and progression of IBD. The dietary flavonoid, kaempferol, has been reported to inhibit expression of inflammatory mediators; however, the underlying mechanisms require further investigation. In the present study, a novel molecular mechanism of kaempferol against IBD was identified. The potential anti‑inflammatory effect of kaempferol in a cellular model of intestinal inflammation was assessed using lipopolysaccharide (LPS)‑induced rat intestinal microvascular endothelial cells (RIMVECs), and an underlying key molecular mechanism was identified. RIMVECs were pretreated with kaempferol of various concentrations (12.5, 25 and 50 µM) followed by LPS (10 µg/ml) stimulation. ELISA was used to examine the protein levels of tumor necrosis factor‑α (TNF‑α), interleukin‑1β (IL‑1β), IL‑6, intercellular adhesion molecule-1 (ICAM‑1) and vascular cell adhesion molecule-1 (VCAM‑1) in the supernatant. Protein expression levels of Toll‑like receptor 4 (TLR4), nuclear factor‑κB (NF‑κB) p65, inhibitor of NF‑κB, mitogen‑activated protein kinase p38 and signal transducer and activator of transcription (STAT) in cells were measured by western blotting. Kaempferol significantly reduced the overproduction of TNF‑α, IL‑1β, interleukin‑6, ICAM‑1 and VCAM‑1 induced by LPS, indicating the negative regulation of kaempferol in TLR4, NF‑κB and STAT signaling underlying intestinal inflammation. The present results provide support for the potential use of kaempferol as an effective therapeutic agent for IBD treatment.
2868 related Products with: Kaempferol inhibits multiple pathways involved in the secretion of inflammatory mediators from LPS‑induced rat intestinal microvascular endothelial cells.Human Large Intestine Mic GLP 2 ELISA Kit, Rat Prog Human Small Intestine Mic GLP 1 ELISA Kit, Rat Gluc Human Pancreatic Microvas Human Tonsil Microvascula Mouse Brain Microvascular Human Glomerular Microvas Human Liver Sinusoidal Mi Human Internal Mammary Ar Human Uterine Microvascul GFP Expressing Human Brai
#30510170 // Save this To Up
Clostridium difficile toxins induce VEGF-A and vascular permeability to promote disease pathogenesis.Clostridium difficile infection (CDI) is mediated by two major exotoxins, toxin A (TcdA) and toxin B (TcdB), that damage the colonic epithelial barrier and induce inflammatory responses. The function of the colonic vascular barrier during CDI has been relatively understudied. Here we report increased colonic vascular permeability in CDI mice and elevated vascular endothelial growth factor A (VEGF-A), which was induced in vivo by infection with TcdA- and/or TcdB-producing C. difficile strains but not with a TcdATcdB isogenic mutant. TcdA or TcdB also induced the expression of VEGF-A in human colonic mucosal biopsies. Hypoxia-inducible factor signalling appeared to mediate toxin-induced VEGF production in colonocytes, which can further stimulate human intestinal microvascular endothelial cells. Both neutralization of VEGF-A and inhibition of its signalling pathway attenuated CDI in vivo. Compared to healthy controls, CDI patients had significantly higher serum VEGF-A that subsequently decreased after treatment. Our findings indicate critical roles for toxin-induced VEGF-A and colonic vascular permeability in CDI pathogenesis and may also point to the pathophysiological significance of the gut vascular barrier in response to virulence factors of enteric pathogens. As an alternative to pathogen-targeted therapy, this study may enable new host-directed therapeutic approaches for severe, refractory CDI.
2373 related Products with: Clostridium difficile toxins induce VEGF-A and vascular permeability to promote disease pathogenesis.Mouse Anti-Clostridium di Mouse Anti-Clostridium di Mouse Anti-Clostridium di FIV Core Ag, recombinant Clostridum difficile toxi Clostridum difficile toxi ENZYMATIC ASSAY KITS (CH Mouse Anti-C. difficile T Clostridum difficile toxi Mouse Anti-Clostridium bo LIVER DISEASES Total Bile Toxoplasma gondii GRA8, r
#29185482 // Save this To Up
A novel role for OATP2A1/SLCO2A1 in a murine model of colon cancer.Prostaglandin E (PGE) is associated with proliferation and angiogenesis in colorectal tumours. The role of prostaglandin transporter OATP2A1/SLCO2A1 in colon cancer tumorogenesis is unknown. We evaluated mice of various Slco2a1 genotypes in a murine model of colon cancer, the adenomatous polyposis (APC) mutant (Apc ) model. Median lifespan was significantly extended from 19 weeks in Slco2a1 /Apc mice to 25 weeks in Slco2a1 /Apc mice. Survival was directly related to a reduction in the number of large polyps in the Slco2a1 /Apc compared to the Slco2a1 /Apc or Slco2a1 /Apc mice. The large polyps from the Slco2a1 /Apc mice had significant reductions in microvascular density, consistent with the high expression of Slco2a1 in the tumour-associated vascular endothelial cells. Chemical suppression of OATP2A1 function significantly reduced tube formation and wound-healing activity of PGE in human vascular endothelial cells (HUVECs) although the amount of extracellular PGE was not affected by an OATP2A1 inhibitor. Further an in vivo model of angiogenesis, showed a significant reduction of haemoglobin content (54.2%) in sponges implanted into Slco2a1 , compared to wildtype mice. These studies indicate that OATP2A1 is likely to promote tumorogenesis by PGE uptake into the endothelial cells, suggesting that blockade of OATP2A1 is an additional pharmacologic strategy to improve colon cancer outcomes.
Colon cancer tissue array Colon cancer survey tissu Colon cancer tissue array Colon cancer tissue array Colon cancer and normal t Colon cancer high density High density colon cancer Colon cancer test tissue Colon cancer and normal c Colon cancer tissue array Colon cancer survey tissu Colon cancer tissue array
#28827082 // Save this To Up
MFSD2A Promotes Endothelial Generation of Inflammation-Resolving Lipid Mediators and Reduces Colitis in Mice.Alterations in signaling pathways that regulate resolution of inflammation (resolving pathways) contribute to pathogenesis of ulcerative colitis (UC). The resolution process is regulated by lipid mediators, such as those derived from the ω-3 docosahexaenoic acid (DHA), whose esterified form is transported by the major facilitator superfamily domain containing 2A (MFSD2A) through the endothelium of brain, retina, and placenta. We investigated if and how MFSD2A regulates lipid metabolism of gut endothelial cells to promote resolution of intestinal inflammation.
1963 related Products with: MFSD2A Promotes Endothelial Generation of Inflammation-Resolving Lipid Mediators and Reduces Colitis in Mice.Androgen Receptor Antibod Goat Anti-Human Endotheli Human Tonsil Microvascula Androgen Receptor Antibod Endothelial Lipase Antibo GFP Expressing Human Saph 5α-N-Acetyl-2'H-androst- Androgen Receptor (Phosph Mouse Brain Microvascular Androsta-1,4,6-triene-3,1 Inflammation (Human) Anti Mouse Anti-Pig Endothelia
#27981571 // Save this To Up
Haematopoietic prolyl hydroxylase-1 deficiency promotes M2 macrophage polarization and is both necessary and sufficient to protect against experimental colitis.Prolyl hydroxylase domain-containing proteins (PHDs) regulate the adaptation of cells to hypoxia. Pan-hydroxylase inhibition is protective in experimental colitis, in which PHD1 plays a prominent role. However, it is currently unknown how PHD1 targeting regulates this protection and which cell type(s) are involved. Here, we demonstrated that Phd1 deletion in endothelial and haematopoietic cells (Phd1 Tie2:cre) protected mice from dextran sulphate sodium (DSS)-induced colitis, with reduced epithelial erosions, immune cell infiltration, and colonic microvascular dysfunction, whereas the response of Phd2 Tie2:cre and Phd3 Tie2:cre mice to DSS was similar to that of their littermate controls. Using bone marrow chimeras and cell-specific cre mice, we demonstrated that ablation of Phd1 in haematopoietic cells but not in endothelial cells was both necessary and sufficient to inhibit experimental colitis. This effect relied, at least in part, on skewing of Phd1-deficient bone marrow-derived macrophages towards an anti-inflammatory M2 phenotype. These cells showed an attenuated nuclear factor-κB-dependent response to lipopolysaccharide (LPS), which in turn diminished endothelial chemokine expression. In addition, Phd1 deficiency in dendritic cells significantly reduced interleukin-1β production in response to LPS. Taken together, our results further support the development of selective PHD1 inhibitors for ulcerative colitis, and identify haematopoietic cells as their primary target. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
2137 related Products with: Haematopoietic prolyl hydroxylase-1 deficiency promotes M2 macrophage polarization and is both necessary and sufficient to protect against experimental colitis.Androgen Receptor (Phosph Recombinant Human Androge Androsta-3,5,16-trien-17- Rabbit Anti-Tyrosine Hydr Androgen Receptor Androgen Receptor 3β-O-Acetyl-androsta-5,1 Anti-Androgen Receptor pr 5α-Androstan-3β-ol � Androgen Receptor , Mouse Androstane 3a, 17b diol 5 Androgen Receptor (Phosph
#25644809 // Save this To Up
Corosolic Acid Exhibits Anti-angiogenic and Anti-lymphangiogenic Effects on In Vitro Endothelial Cells and on an In Vivo CT-26 Colon Carcinoma Animal Model.We describe the anti-angiogenic and anti-lymphangiogenic effects of corosolic acid, a pentacyclic triterpenoid isolated from Cornus kousa Burg. A mouse colon carcinoma CT-26 animal model was employed to determine the in vivo anti-angiogenic and anti-lymphangiogenic effects of corosolic acid. Corosolic acid induced apoptosis in CT-26 cells, mediated by the activation of caspase-3. In addition, it reduced the final tumor volume and the blood and lymphatic vessel densities of tumors, indicating that it suppresses in vivo angiogenesis and lymphangiogenesis. Corosolic acid inhibited the proliferation and tube formation of human umbilical vein endothelial cells and human dermal lymphatic microvascular endothelial cells. In addition, corosolic acid decreased the proliferation and migration of human umbilical vein endothelial cells stimulated by angiopoietin-1. Pretreatment with corosolic acid decreased the phosphorylation of focal adhesion kinase (FAK) and ERK1/2, suggesting that corosolic acid contains anti-angiogenic activity that can suppress FAK signaling induced by angiopoietin-1.
2725 related Products with: Corosolic Acid Exhibits Anti-angiogenic and Anti-lymphangiogenic Effects on In Vitro Endothelial Cells and on an In Vivo CT-26 Colon Carcinoma Animal Model.Colon carcinoma tissue ar Colon carcinoma tissue ar Rabbit Anti-FGF3 Oncogene Colon adenocarcinoma with Colon cancer tissue array Rabbit Anti-IAA (Indole-3 Rabbit Anti-IAA (Indole-3 Hepatocellular carcinoma Proteins and Antibodies H Colon cancer tissue array Rabbit Anti-IAA (Indole-3 Rabbit Anti-IAA (Indole-3
#25307345 // Save this To Up
The neurotensin-HIF-1α-VEGFα axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis.The expression of neurotensin (NT) and its receptor (NTR1) is up-regulated in experimental colitis and inflammatory bowel disease; NT/NTR1 interactions regulate gut inflammation. During active inflammation, metabolic shifts toward hypoxia lead to the activation of hypoxia-inducible factor (HIF)-1, which enhances vascular endothelial growth factor (VEGF) expression, promoting angiogenesis. We hypothesized that NT/NTR1 signaling regulates intestinal manifestations of hypoxia and angiogenesis by promoting HIF-1 transcriptional activity and VEGFα expression in experimental colitis. We studied NTR1 signaling in colitis-associated angiogenesis using 2,4,6-trinitrobenzenesulfonic acid-treated wild-type and NTR1-knockout mice. The effects of NT on HIF-1α and VEGFα were assessed on human colonic epithelial cells overexpressing NTR1 (NCM460-NTR1) and human intestinal microvascular-endothelial cells. NTR1-knockout mice had reduced microvascular density and mucosal integrity score compared with wild-type mice after 2,4,6-trinitrobenzenesulfonic acid treatment. VEGFα mRNA levels were increased in NCM460-NTR1 cells treated with 10(-7) mol/L NT, at 1 and 6 hours post-treatment. NT exposure in NCM460-NTR1 cells caused stabilization, nuclear translocation, and transcriptional activity of HIF-1α in a diacylglycerol kinase-dependent manner. NT did not stimulate tube formation in isolated human intestinal macrovascular endothelial cells but did so in human intestinal macrovascular endothelial cells cocultured with NCM460-NTR1 cells. Our results demonstrate the importance of an NTR1-HIF-1α-VEGFα axis in intestinal angiogenic responses and in the pathophysiology of colitis and inflammatory bowel disease.
1250 related Products with: The neurotensin-HIF-1α-VEGFα axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis.Thermostable TDG Kit (DIS 19 Hydroxy 4 androstene 3 Rabbit Anti-Human Androge Esophageal inflammation, Rabbit anti PKC theta (Ab Angiogenesis (Human) Anti Theobromine CAS Number [8 Androgen Receptor (Phosph Angiogenesis (Human) Quan FDA Standard Frozen Tissu Monoclonal Anti-Alkaline Human Inflammation Array
#24914216 // Save this To Up
Differential effects of Escherichia coli subtilase cytotoxin and Shiga toxin 2 on chemokine and proinflammatory cytokine expression in human macrophage, colonic epithelial, and brain microvascular endothelial cell lines.Subtilase cytotoxin (SubAB) is the prototype of a recently emerged family of AB5 cytotoxins produced by Shiga-toxigenic Escherichia coli (STEC). Its mechanism of action involves highly specific A-subunit-mediated proteolytic cleavage of the essential endoplasmic reticulum (ER) chaperone BiP. Our previous in vivo studies showed that intraperitoneal injection of purified SubAB causes a major redistribution of leukocytes and elevated leukocyte apoptosis in mice, as well as profound splenic atrophy. In the current study, we investigated selected chemokine and proinflammatory cytokine responses to treatment with SubAB, a nontoxic derivative (SubAA272B), or Shiga toxin 2 (Stx2) in human macrophage (U937), brain microvascular endothelial (HBMEC), and colonic epithelial (HCT-8) cell lines, at the levels of secreted protein, cell-associated protein, and gene expression. Stx2 treatment upregulated expression of chemokines and cytokines at both the protein and mRNA levels. In contrast, SubAB induced significant decreases in secreted interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) in all three tested cell lines and a significant decrease in secreted IL-6 in HBMECs. The downregulation of secreted chemokines or cytokines was not observed in SubAA272B-treated cells, indicating a requirement for BiP cleavage. The downregulation of secreted chemokines and cytokines by SubAB was not reflected at the mRNA and cell-associated protein levels, suggesting a SubAB-induced export defect.
1302 related Products with: Differential effects of Escherichia coli subtilase cytotoxin and Shiga toxin 2 on chemokine and proinflammatory cytokine expression in human macrophage, colonic epithelial, and brain microvascular endothelial cell lines.Macrophage Colony Stimula Human Brain Microvascular Human Large Intestine Mic Macrophage Colony Stimula GFP Expressing Human Brai Human Small Intestine Mic GFP Expressing Mouse Brai RFP Expressing Human Glom Human Pancreatic Microvas Human Tonsil Microvascula Androgen Receptor Androgen Receptor Ab 1
#24682411 // Save this To Up
Regulated expression of leukocyte-specific transcript (LST) 1 in human intestinal inflammation.Leukocyte-specific transcript 1 (LST1) encoded peptides are involved in immunomodulation and nanotube-mediated cell-cell communication. The aim of this study was to assess the expression of LST1 in colonic epithelium and endothelium during intestinal inflammation.
2823 related Products with: Regulated expression of leukocyte-specific transcript (LST) 1 in human intestinal inflammation.Inflammation (Human) Anti Rabbit Anti-intestinal FA Inflammation (Human) Anti Inflammation (Human) Anti alkaline phosphatase (int Inflammation (Human) Anti Inflammation (Human) Quan Anti-human C1 Esterase In Human Inflammation Array Rabbit Anti-intestinal FA Rabbit Anti-intestinal FA Rabbit Anti-Human Vasoact
#23263571 // Save this To Up
Effective treatment of mouse sepsis with an inhibitory antibody targeting integrin αvβ5.Integrin αvβ5 has been identified as a regulator of vascular leak and endothelial permeability. We hypothesized that targeting αvβ5 could represent a viable treatment strategy for sepsis.
2868 related Products with: Effective treatment of mouse sepsis with an inhibitory antibody targeting integrin αvβ5.Integrin β1 (CD29) Antib Inhibitory mouse monoclo Rabbit Anti-RRAS Polyclon Rabbit Anti-PIWIL4 Polycl Rabbit Anti-Eph receptor Monoclonal Anti-Brain-der Mouse Anti-Insulin(1D4 ) Mouse Anti-Human Bax-UNLB Anti-Human IgG (H+L)mous Monoclonal Anti-dEGF Rece Purified Mouse Anti Human Mouse Anti-Insulin(1D4 )
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia