Tissue engineered pre-vascularized buccal mucosa equivalents utilizing a primary triculture of epithelial cells, endothelial cells and fibroblasts

Biomaterials ◽  
2016 ◽  
Vol 77 ◽  
pp. 207-215 ◽  
Author(s):  
M. Heller ◽  
E.V. Frerick-Ochs ◽  
H.-K. Bauer ◽  
E. Schiegnitz ◽  
D. Flesch ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Buccal Mucosa

CD40 amplifies Fas-mediated apoptosis: a mechanism contributing to emphysema

2012 ◽  
Vol 303 (2) ◽  
pp. L141-L151 ◽  
Author(s):  
Ayako Shigeta ◽  
Yuji Tada ◽  
Ji-Yang Wang ◽  
Shunsuke Ishizaki ◽  
Junichi Tsuyusaki ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Pulmonary Emphysema ◽  
Alveolar Epithelial Cells ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Cd40 Stimulation ◽  
Ifn Γ ◽  
Apoptosis And Inflammation

Excessive apoptosis and prolonged inflammation of alveolar cells are associated with the pathogenesis of pulmonary emphysema. We aimed to determine whether CD40 affects alveolar epithelial cells and endothelial cells, with regard to evoking apoptosis and inflammation. Mice were repeatedly treated with agonistic-anti CD40 antibody (Ab), with or without agonistic-anti Fas Ab, and evaluated for apoptosis and inflammation in lungs. Human pulmonary microvascular endothelial cells and alveolar epithelial cells were treated with agonistic anti-CD40 Ab and/or anti-Fas Ab to see their direct effect on apoptosis and secretion of proinflammatory molecules in vitro. Furthermore, plasma soluble CD40 ligand (sCD40L) level was evaluated in patients with chronic obstructive pulmonary disease (COPD). In mice, inhaling agonistic anti-CD40 Ab induced moderate alveolar enlargement. CD40 stimulation, in combination with anti-Fas Ab, induced significant emphysematous changes and increased alveolar cell apoptosis. CD40 stimulation also enhanced IFN-γ-mediated emphysematous changes, not via apoptosis induction, but via inflammation with lymphocyte accumulation. In vitro, Fas-mediated apoptosis was enhanced by CD40 stimulation and IFN-γ in endothelial cells and by CD40 stimulation in epithelial cells. CD40 stimulation induced secretion of CCR5 ligands in endothelial cells, enhanced with IFN-γ. Plasma sCD40L levels were significantly increased in patients with COPD, inversely correlating to the percentage of forced expiratory volume in 1 s and positively correlating to low attenuation area score by CT scan, regardless of smoking history. Collectively CD40 plays a contributing role in the development of pulmonary emphysema by sensitizing Fas-mediated apoptosis in alveolar cells and increasing the secretion of proinflammatory chemokines.

Disparate cytokine regulation of ICAM-1 in rat alveolar epithelial cells and pulmonary endothelial cells in vitro

1995 ◽  
Vol 269 (1) ◽  
pp. L127-L135 ◽  
Author(s):  
W. W. Barton ◽  
S. Wilcoxen ◽  
P. J. Christensen ◽  
R. Paine
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Inflammatory Cytokines ◽  
Alveolar Epithelial Cells ◽  
Normal Lung ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial

Intercellular adhesion molecule-1 (ICAM-1) is expressed at high levels on type I alveolar epithelial cells in the normal lung and is induced in vitro as type II cells spread in primary culture. In contrast, in most nonhematopoetic cells ICAM-1 expression is induced in response to inflammatory cytokines. We have formed the hypothesis that the signals that control ICAM-1 expression in alveolar epithelial cells are fundamentally different from those controlling expression in most other cells. To test this hypothesis, we have investigated the influence of inflammatory cytokines on ICAM-1 expression in isolated type II cells that have spread in culture and compared this response to that of rat pulmonary artery endothelial cells (RPAEC). ICAM-1 protein, determined both by a cell-based enzyme-linked immunosorbent assay and by Western blot analysis, and mRNA were minimally expressed in unstimulated RPAEC but were significantly induced in a time- and dose-dependent manner by treatment with tumor necrosis factor-alpha, interleukin-1 beta, or interferon-gamma. In contrast, these cytokines did not influence the constitutive high level ICAM-1 protein expression in alveolar epithelial cells and only minimally affected steady-state mRNA levels. ICAM-1 mRNA half-life, measured in the presence of actinomycin D, was relatively long at 7 h in alveolar epithelial cells and 4 h in RPAEC. The striking lack of response of ICAM-1 expression by alveolar epithelial cells to inflammatory cytokines is in contrast to virtually all other epithelial cells studied to date and supports the hypothesis that ICAM-1 expression by these cells is a function of cellular differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The Damage Sensory Molecule TRPA1 Positively Regulates Endogenous Thymic Regeneration after Damage

Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 67-67
Author(s):  
Kimon Argyropoulos ◽  
Enrico Velardi ◽  
Jennifer Tsai ◽  
Amina Lazrak ◽  
Lorenz Jahn ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Epithelial Cells ◽  
Thymic Epithelial Cells ◽  
Lipid Peroxidation Products ◽  
Positive Effects ◽  
Damage Sensing ◽  
Cell Counts ◽  
Thymic Regeneration

Abstract The thymus is extremely sensitive to exogenous insults but has a remarkable capacity to regenerate which is lost with age. Reactive oxygen species (ROS) accumulate early after tissue damage and despite their toxic potential, ROS and their byproducts (such as lipid peroxidation products-LPPs) can act as regeneration signals by activating membrane or intracellular sensors and subsequent stress-response signalling pathways. Using Sublethal Total Body Irradiation (SL-TBI) as a model of acute thymic injury, we found a rapid accumulation of thymic ROS as well as lipid peroxidation products on cell membranes after SLTBI (Figure 1A&B). The damage-sensing ion channel Transient Receptor Potential cation channel family A member 1 (TRPA1) represents one of the major damage sensing receptors that can mediate cellular responses to oxidative stress mediators, such as LPPs. Using immunofluorescence (IF) microscopy we found that TRPA1 is enriched in the thymic medulla. Interestingly, although TRPA1 has been classically identified in nociceptive fibers, the major TRPA1 expressing structures in the thymus were not nerve fiber terminals, but primarily thymic endothelial cells (Figure1C), fibroblasts and subsets of epithelial cells. We have recently demonstrated that thymic endothelial cells can regulate regeneration through secretion of BMP-4, which can enhance Foxn1 expression and proliferation of thymic epithelial cells. In order to assess the functional role of TRPA1 in thymic regeneration after injury, we utilized TRPA1 knockout (TRPA1-/-) mice and quantified thymic reconstitution after SL-TBI. TRPA1-/- mice had significantly lower thymic cellularity compared to their age- and sex-matched WT controls, suggesting an association between TRPA1 deficiency and delayed endogenous thymic recovery (Figure 1D). The major deficit in thymocyte counts primarily affected double negative-4 (DN4), double positive (DP) and CD4+ single positive (SP-CD4+) thymocyte numbers. The thymic stroma of TRPA1-/- mice had lower endothelial cell and fibroblast counts (Figure 1D). In accordance with these findings drinking water administration of the TRPA1 agonist Allyl-Isothiocyanate (AITC), resulted in enhanced thymic regeneration after radiation exposure. Besides its positive effects on thymocyte counts, AITC significantly augmented endothelial cell counts after irradiation (Figure 1E). In conclusion these results suggest that TRPA1 plays a non-redundant role in thymic regeneration and that exogenous TRPA1 stimulation can enhance immune recovery after damage. Disclosures van den Brink: Seres: Research Funding; Jazz Pharmaceuticals: Consultancy; PureTech Health: Consultancy; Therakos Institute: Other: Speaking engagement.

Peroxiredoxin I expression in epithelial cells of buccal mucosa from patients exposed to panoramic X-rays: influence of the age

2017 ◽  
Vol 22 (3) ◽  
pp. 1587-1592 ◽  
Author(s):  
Milena B. Silva ◽  
Ana P. D. Demasi ◽  
Elizabeth F. Martinez ◽  
Maristane L. Goudinho ◽  
Joarlene M. Soares ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Buccal Mucosa ◽  
X Rays ◽  
Peroxiredoxin I

scholarly journals Cytokine-Mediated Downregulation of Coxsackievirus-Adenovirus Receptor in Endothelial Cells

2004 ◽  
Vol 78 (15) ◽  
pp. 8047-8058 ◽  
Author(s):  
Theresa Vincent ◽  
Ralf F. Pettersson ◽  
Ronald G. Crystal ◽  
Philip L. Leopold
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Western Blot ◽  
Inflammatory Cytokines ◽  
Cell Physiology ◽  
Mrna Levels ◽  
Cytokine Treatment ◽  
Adenovirus Receptor ◽  
The Impact

ABSTRACT Endothelial cells have the ability to change their complement of cell surface proteins in response to inflammatory cytokines. We hypothesized that the expression of the coxsackievirus-adenovirus receptor (CAR), a viral receptor and putative cell-cell adhesion molecule, may be altered during the response of endothelial cells to inflammation. To test this hypothesis, we evaluated CAR protein and mRNA levels in human umbilical vein endothelial cells after they were exposed to tumor necrosis factor alpha, gamma interferon, or a combination of the two cytokines. Flow cytometric and Western blot analyses indicated that cytokine treatment led to a synergistic decrease in CAR protein expression. A Western blot analysis showed that CAR levels decreased to 16% ± 4% or 1% ± 4% of the CAR protein levels in untreated cells with either 24 or 48 h of cytokine treatment, respectively. Quantitative reverse transcription-PCR demonstrated that the combination treatment caused CAR mRNA levels to decrease to 21% ± 12% or 5% ± 3% of the levels in untreated cells after a 24- or 48-h cytokine treatment, respectively. Reduced CAR expression led to a decrease in adenovirus (Ad) binding of 80% ± 3% (compared with untreated endothelial cells), with a subsequent decrease in Ad-mediated gene transfer that was dependent on the dose and duration of cytokine treatment but not on the dose of Ad. A similar decrease in CAR protein level and susceptibility to Ad infection was observed in human microvascular endothelial cells, while CAR expression on normal human bronchial epithelial cells or A549 lung epithelial cells was less affected by cytokine treatments. Taken together, the data demonstrate that inflammatory cytokines decrease CAR mRNA and protein expression with a concomitant decrease in Ad binding, reflecting the impact of cell physiology on the function of CAR and the potential effect of inflammation on the ability of Ad to transfer genes to endothelial cells.

scholarly journals Expression of claudins in the normal canine gastric mucosa

2014 ◽  
Vol 62 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Roland Psáder ◽  
Csaba Jakab ◽  
Ákos Máthé ◽  
Gyula Balka ◽  
Kinga Pápa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Apical Part ◽  
Basal Part ◽  
Gastric Epithelial Cells ◽  
Gastric Glands ◽  
Gastric Cells ◽  
Pyloric Stomach ◽  
Mucous Neck Cells

The aim of the present study was to investigate the expression pattern of claudin-1, -2, -3, -4, -5, -7, -8, -10 and -18 in the intact fundic and pyloric gastric mucosa of dogs. Intense, linear, membranous claudin-18 positivity was detected in the surface gastric cells and in the epithelial cells of the gastric glands both in the fundic and pyloric stomach regions. The mucous neck cells in the apical part of the glands, furthermore the parietal cells and chief cells of the basal part of the gland were all positive for claudin-18, in the same way as the enteroendocrine cells. Cells of the basal part of the pyloric glands showed intense, linear, membranous claudin-2 positivity, but cells of the superficial portion of these glands and the surface gastric cells in this region were claudin-2 negative. Fibroblasts, endothelial cells, lymphocytes of the propria layer, smooth muscle cells and vegetative neurons were all negative for claudin-2. All gastric epithelial cells were negative for claudin-1, -3, -4, -5, -6, -7, -8 and -10. The endothelial cells of the propria layer had intense claudin-5 positivity. We assume that claudin-18 forms a paracellular barrier against gastric acid in the healthy canine stomach, in the same way as in mice.

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