Search results for: Human Bladder Microvascular Endothelial Cells
#30843693 // Save this To Up
An Air-Liquid Interface Organ-Level Lung Microfluidics Platform for Analysis on Molecular Mechanisms of Cytotoxicity Induced by Cancer-Causing Fine Particles.Fine particulate matter less than 2.5 μm in diameter (PM) is regarded as a carcinogenic factor, but the mechanism has been left unexplored. Our goal was to reveal the carcinogenic mechanism at the gene and protein level under the inhalational air-liquid interface (ALI) condition. Herein, we developed an ALI organ-level lung microfluidic platform (ALI-OLMP) carrying lung epithelial cell line BEAS-2B and human pulmonary microvascular endothelial cells (HPMEC); the cell viability was above 98% within 14 days on this system, which was used to mimic the practical alveolar microenvironment for the multiomics analysis, to identify the global gene and protein expression after exposure to PM in Shanghai, China from 2014 to 2015. The combined RNA-Seq and iTRAQ analysis indicated that the unique set was 2532 genes at 10 μg/cm of PM, and there were also at least 25 identical activated signal transduction cascades including bladder cancer, transcriptional dysregulation in cancer, the TP53 (p53) signaling pathway, Jak-STAT signaling pathway, and PI3K-Akt signaling pathway, which could lead to blocking of differentiation, cell proliferation and survival, and sustained angiogenesis. The images obtained by the transmission electron microscopy (TEM) showed that the particles could enter the mitochondria, and even get into the nucleus. The Pearson's correlation coefficient test elucidated that inorganics (EC), organics (OC, PAHs, and alkane), and metals (Cr, Mn, and Sb) were significantly correlated to the dysregulated oncoproteins (VEGF, IL6, MDM2, AKT1, STAT, and P53). The findings may to some extent explain the molecular mechanism of carcinogenicity caused by fine-particle exposure.
2737 related Products with: An Air-Liquid Interface Organ-Level Lung Microfluidics Platform for Analysis on Molecular Mechanisms of Cytotoxicity Induced by Cancer-Causing Fine Particles.Lung cancer tissue array, Multiple organ cancer fro Frozen multiple organ can Lung cancer tissue array Lung cancer test tissue a Multiple organ cancer tis Multiple organ cancer fro Multiple organ cancer fro Lung cancer tissue array, Lung cancer tissue array, Lung cancer tissue array, Multiple organ cancer fro
#28220552 // Save this To Up
Activation of the mTOR dependent signaling pathway underlies ketamine-induced uropathy.To investigate the pathogenic role of activation of the mammalian target of the rapamycin (mTOR) in the ketamine induced microvascular injury.
2679 related Products with: Activation of the mTOR dependent signaling pathway underlies ketamine-induced uropathy.PathwayReady™ PI3 K Akt TGF-Beta Signaling Phosph AP-1 Reporter – HEK293 Anti-AICDA(Activation-ind p53 Signaling Phospho-Spe ERK Signaling Phospho-Spe mTOR Signalign Phospho-Sp AMPK Signaling Phospho-Sp PathwayReady™ EGFR Sign T-Cell Receptor Signaling DiscoveryPak™ Hedgehog IGF-1R Signaling Phospho-
#27816993 // Save this To Up
Adhesion of Escherichia coli under flow conditions reveals potential novel effects of FimH mutations.FimH-mediated adhesion of Escherichia coli to bladder epithelium is a prerequisite for urinary tract infections. FimH is also essential for blood-borne bacterial dissemination, but the mechanisms are poorly understood. The purpose of this study was to assess the influence of different FimH mutations on bacterial adhesion using a novel adhesion assay, which models the physiological flow conditions bacteria are exposed to. We introduced 12 different point mutations in the mannose binding pocket of FimH in an E. coli strain expressing type 1 fimbriae only (MSC95-FimH). We compared the bacterial adhesion of each mutant across several commonly used adhesion assays, including agglutination of yeast, adhesion to mono- and tri-mannosylated substrates, and static adhesion to bladder epithelial and endothelial cells. We performed a comparison of these assays to a novel method that we developed to study bacterial adhesion to mammalian cells under flow conditions. We showed that E. coli MSC95-FimH adheres more efficiently to microvascular endothelium than to bladder epithelium, and that only endothelium supports adhesion at physiological shear stress. The results confirmed that mannose binding pocket mutations abrogated adhesion. We demonstrated that FimH residues E50 and T53 are crucial for adhesion under flow conditions. The coating of endothelial cells on biochips and modelling of physiological flow conditions enabled us to identify FimH residues crucial for adhesion. These results provide novel insights into screening methods to determine the effect of FimH mutants and potentially FimH antagonists.
2793 related Products with: Adhesion of Escherichia coli under flow conditions reveals potential novel effects of FimH mutations.Mouse Anti-Escherichia co Cell Meter™ NIR Mitocho ESCHERICHIA COLI clinical Mouse Anti-Escherichia co Mouse Anti-Escherichia co Mouse Anti-Escherichia co Cell Meter™ Mitochondri Rabbit Anti-E.coli O6 Pol Mouse Anti-Escherichia co Cell Meter™ JC 10 Mitoc Goat Anti-Escherichia col Mouse Anti-Escherichia co
#27529746 // Save this To Up
Microvascular Injury in Ketamine-Induced Bladder Dysfunction.The pathogenesis of ketamine-induced cystitis (KC) remains unclear. In this study, bladder microvascular injury was investigated as a possible contributing mechanism. A total of 36 KC patients with exposure to ketamine for more than 6 months, and 9 control subjects, were prospectively recruited. All participants completed questionnaires, including the O'Leary-Sant interstitial cystitis symptom index (ICSI) and the interstitial cystitis problem index (ICPI). All KC patients received a urodynamic study and radiological exams. Bladder tissues were obtained from cystoscopic biopsies in the control group and after hydrodistention in the KC group. Double-immunofluorescence staining of N-methyl-d-aspartate receptor subunit 1 (NMDAR1) and the endothelial marker, cluster of differentiation 31 (CD31), was performed to reveal the existence of NMDAR1 on the endothelium. Electron microscopy (EM) was applied to assess the microvascular change in the urinary bladder and to measure the thickening of the basement membrane (BM). A proximity ligation assay (PLA) was used to quantify the co-localization of the endothelial CD31 receptor and the mesenchymal marker [fibroblast-specific protein 1 (FSP-1)]. The Mann-Whitney U test and Spearman's correlation coefficient were used for statistical analysis. The mean ICSI [14.38 (± 4.16)] and ICPI [12.67 (± 3.54)] scores of the KC group were significantly higher than those (0 and 0, respectively) of the control group (both p < 0.001). The KC patients had decreasing cystometric bladder capacity (CBC) with a mean volume of 65.38 (± 48.67) mL. NMDAR1 was expressed on endothelial cells in both groups under immunofluorescence staining. Moreover, KC patients had significant BM duplication of microvessels in the mucosa of the urinary bladder under EM. The co-expression of the endothelial marker CD31 and mesenchymal marker FSP1 was significantly stained and calculated under PLA. In conclusion, microvascular injury and mesenchymal phenotypic alteration of endothelial cells can potentially contribute to KC-induced bladder dysfunction.
Bladder cancer tissue arr Human Large Intestine Mic Anti AGO2 Human, Monoclon Human Kidney injury molec Jurkat Cell Extract (Indu Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer test tissu Jurkat Cell Extract (Indu Human Bladder Microvascul Anti AGO2 Human, Monoclon
#26854200 // Save this To Up
Co-delivery of VEGF and bFGF via a PLGA nanoparticle-modified BAM for effective contracture inhibition of regenerated bladder tissue in rabbits.Graft contracture is a common problem associated with the regeneration processes of tissue-engineered bladders. Currently, most strategies used for incorporating bioactive molecules into biomaterial designs do not work during all phases of tissue regeneration. In this study, we used a growth factor-PLGA nanoparticle thermo-sensitive gel system (i.e., BAM with incorporated VEGF and bFGF-loaded PLGA nanoparticles and mixed with a hydrophilic gel) to promote bladder tissue regeneration in a rabbit model. At 4 and 12 weeks after surgery, contracture rate assessment and histological examination were conducted to evaluate bladder tissue regeneration. The results indicated that the functional composite scaffold continuously and effectively released VEGF and bFGF and promoted bladder reconstruction with a significant decrease in graft contracture. In addition, the number and arrangement of regenerated urothelial cells and smooth muscle cells as well as microvascular density and maturity were improved in the VEGF/bFGF nanoparticle group compared with the single factor VEGF or bFGF nanoparticle group and BAM alone. The nanoparticle thermo-sensitive gel system, which exhibited favourable performance, may effectively inhibit graft contracture and promote bladder tissue regeneration in rabbits.
2244 related Products with: Co-delivery of VEGF and bFGF via a PLGA nanoparticle-modified BAM for effective contracture inhibition of regenerated bladder tissue in rabbits.Mid advanced stage bladde Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer test tissu Multiple lung carcinoma ( GI cancer (esophageal, ga Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer test tissu
#26414101 // Save this To Up
Tissue-Engineered Microvasculature to Reperfuse Isolated Renal Glomeruli.Kidney transplantation is often the most effective therapy for end-stage renal disease, but there are not enough donor organs to meet the rising demand. Tissue engineering of kidneys is a potential solution to this organ shortage. Achieving microvascular perfusion has been a major barrier to engineering tissues beyond thin muscularized sheets such as the bladder wall. Our laboratory has previously reported that human umbilical vein endothelial cells (ECs) transduced with the antiapoptotic protein Bcl-2 will spontaneously organize into perfused microvessels within type I collagen gels when implanted in immunodeficient mice. To test if this system can be used to perfuse more complex structures, we combined Bcl-2-transduced ECs (Bcl-2-ECs) with renal glomeruli, the specialized vascular filtration units of the kidney. Microdissected green fluorescent protein-expressing rat glomeruli suspended in type I collagen gels were implanted within immunodeficient mice with or without the inclusion of Bcl-2-ECs. Survival of rat glomeruli was enhanced by coimplantation with Bcl-2-ECs. Intravital rhodamine dextran injections demonstrated that surviving glomeruli were perfused through Bcl-2-EC-derived microvessels. Perfused glomeruli maintained podocin staining, but transmission electron microscopy revealed endothelial swelling and podocyte foot process effacement. Anastomosis of microvessels derived from Bcl-2-ECs with glomerular capillaries provides proof of concept that self-assembled microvessels can perfuse specialized organ structures such as glomeruli, but that perfusion alone may be insufficient to maintain normal structure.
2391 related Products with: Tissue-Engineered Microvasculature to Reperfuse Isolated Renal Glomeruli.Kidney cancer test tissue Oral cavity (tongue and p FDA Standard Frozen Tissu Head & Neck cancer test t Tonsil disease spectrum ( FDA Standard Frozen Tissu Total RNA - Human Tumor T Oral squamous cell cancer FDA Standard Frozen Tissu Kidney disease spectrum ( Rat Tissue Lysate (total Renal disease spectrum ti
#26129954 // Save this To Up
Expression of brain‑specific angiogenesis inhibitor‑1 and association with p53, microvessel density and vascular endothelial growth factor in the tissue of human bladder transitional cell carcinoma.The aim of the present study was to investigate the expression levels of brain‑specific angiogenesis inhibitor‑1 (BAI‑1) in bladder transitional cell carcinoma (BTCC) at different stages and the mechanism by which it inhibits tumor endothelial cell proliferation. Normal bladder mucosa biopsy specimens were obtained as the control group, and human BTCC biopsy specimens were used as the study group. Immunohistochemical assays were used to detect the expression levels of BAI‑1, vascular endothelial growth factor (VEGF) and mutant p53, in addition to microvessel density (MVD) in the tissues. Western blotting was used to analyze the differential expression of BAI‑1 in the two samples. Statistical analysis was performed, which indicated that BAI‑1 expression levels in the normal bladder mucosa group were significantly higher than those in the BTCC group and were associated with clinical staging. BAI‑1 levels in the T1 stage BTCC tissues were higher than those in the T2‑4 stage BTCC tissues (P<0.05). BAI‑1 expression levels were negatively correlated with those of VEGF (r=‑0.661, P<0.001), mutant p53 (r=‑0.406, P=0.002) and with the MVD (r=‑0.675, P<0.001). BAI‑1 may be involved in the negative regulation of BTCC microvascular proliferation, and its expression may be associated with a reduction in p53 mutations.
1345 related Products with: Expression of brain‑specific angiogenesis inhibitor‑1 and association with p53, microvessel density and vascular endothelial growth factor in the tissue of human bladder transitional cell carcinoma.Brain Specific Angiogenes Brain-Specific Angiogenes Goat Anti-Human Tissue Fa Growth Factor (Human) Ant Human Endocrine Gland Vas High density non small ce Recombinant Human Vascula Oral cavity squamous cell Human Vascular Endothelia Human Vascular Endothelia Human Insulin-like Growth Mouse Vascular Endothelia
#24055455 // Save this To Up
The effect of detergents on the basement membrane complex of a biologic scaffold material.The basement membrane complex (BMC) is a critical component of the extracellular matrix (ECM) that supports and facilitates the growth of cells. This study investigates four detergents commonly used in the process of tissue decellularization and their effect upon the BMC. The BMC of porcine urinary bladder was subjected to 3% Triton-X 100, 8mM 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS), 4% sodium deoxycholate or 1% sodium dodecyl sulfate (SDS) for 24h. The BMC structure for each treatment group was assessed by immunolabeling, scanning electron microscopy (SEM) and second harmonic generation (SHG) imaging of the fiber network. The composition was assessed by quantification of dsDNA, glycosaminoglycans (GAG) and collagen content. The results showed that collagen fibers within samples treated with 1% SDS and 8mM CHAPS were denatured, and the ECM contained fewer GAG compared with samples treated with 3% Triton X-100 or 4% sodium deoxycholate. Human microvascular endothelial cells (HMEC) were seeded onto each BMC and cultured for 7 days. Cell-ECM interactions were investigated by immunolabeling for integrin β-1, SEM imaging and semi-quantitative assessment of cellular infiltration, phenotype and confluence. HMEC cultured on a BMC treated with 3% Triton X-100 were more confluent and had a normal phenotype compared with HMEC cultured on a BMC treated with 4% sodium deoxycholate, 8mM CHAPS and 1% SDS. Both 8mM CHAPS and 1% SDS damaged the BMC to the extent that seeded HMEC were able to infiltrate the damaged sub-basement membrane tissue, showed decreased confluence and an atypical phenotype. The choice of detergents used for tissue decellularization can have a marked effect upon the integrity of the BMC of the resultant bioscaffold.
1196 related Products with: The effect of detergents on the basement membrane complex of a biologic scaffold material.Thermal Shaker with cooli Anti-basement membrane ma FDA Standard Frozen Tissu Normal rat multiple organ TCP-1 theta antibody Sour Rabbit anti PKC theta (pS Sheep Anti-Theophylline 3 FDA Standard Frozen Tissu Rabbit anti PKC theta (Ab Tissue array of ovarian g FDA Standard Frozen Tissu Multiple organ cancer tis
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