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1.
Fig. 5

Fig. 5. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Activation of hypoxic-inducible factor attenuates inflammatory mediator expression. Similar as in experiments using exposure to hypoxia (5% oxygen), inflammatory mediator secretion is attenuated (P < 0·001) in alveolar epithelial cells (AEC) stimulated with 1 mM N-(methoxyoxoacetyl)-glycine methyl ester [dimethyloxalyl glycine (DMOG), an inhibitor of prolyl-4-hydroxylase]. CINC-1, cytokine-induced neutrophil chemoattractant-1; MCP-1, monocyte chemoattractant protein-1.

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.
2.
Fig. 4

Fig. 4. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Alveolar macrophages. Production of inflammatory mediators from alveolar macrophages (MAC) under hypoxic and normoxic conditions, with or without dexamethasone pretreatment: both hypoxic conditions and dexamethasone treatment decreased monocyte chemoattractant protein-1 (MCP-1) protein concentration (P < 0·001), as well as MCP-1 and intercellular adhesion molecule-1 (ICAM-1) mRNA levels (P < 0·05) in alveolar macrophages. Cytokine-induced neutrophil chemoattractant-1 and interleukin (IL)-6 protein was not detectable in supernatants.

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.
3.
Fig. 7

Fig. 7. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Viability. Alveolar epithelial cells (AEC) rat pulmonary artery endothelial cells (RPAEC), and alveolar macrophages (MAC) were pretreated with dexamethasone (or not) and exposed to 5% oxygen (or 21% as control) for 24 h. Dimethylthiozol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assays were performed: no influences of variations in viability on inflammatory mediator expression or ion fluxes were found.

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.
4.
Fig. 6

Fig. 6. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Ion channel expression and function. Expression of apical epithelial sodium channel (αENaC) and basolateral Na+/K+-ATPase (mRNA-expression, left) with corresponding actual channel turnover measured by radioactive tracer ions (amiloride-sensitive 22Na uptake for ENaC function, ouabain-sensitive 86rubidium uptake for Na+/K+-ATPase function, right). Total 22Na flux was decreased after exposure to hypoxia (P < 0·001). When pre-incubated with dexamethasone, 22Na flux was partially maintained (P = 0·001). In contrast, no increased 86rubidium uptake upon dexamethasone treatment was observed. Co, control, Hyp, hypoxia, Dex, dexamethasone.

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.
5.
Fig. 2

Fig. 2. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Alveolar epithelial cells (AEC). Production of inflammatory mediators from alveolar epithelial cells type II (L2, AEC) under hypoxic and normoxic conditions, with or without dexamethasone pretreatment: protein concentrations in supernatants (left) and mRNA expression levels (right). Hypoxia decreased cytokine-induced neutrophil chemoattractant-1 (CINC-1) and monocyte chemoattractant protein-1 (MCP-1) expression (P < 0·001), but not interleukin (IL)-6 protein secretion (P = 0·08). Addition of dexamethasone under hypoxic conditions attenuated CINC-1 and MCP-1 levels even more (P < 0·001).

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.
6.
Fig. 3

Fig. 3. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Rat pulmonary artery endothelial cells. Production of inflammatory mediators from rat pulmonary endothelial cells (RPAEC) under hypoxic and normoxic conditions, with or without dexamethasone pretreatment: protein concentrations in supernatants (left) and mRNA expression levels (right). Hypoxia decreased cytokine-induced neutrophil chemoattractant-1 (CINC-1) (P < 0·001), but not monocyte chemoattractant protein-1 (MCP-1) or interleukin (IL)-6 protein expression. Dexamethasone attenuated MCP-1 secretion under normoxic and hypoxic conditions (P < 0·001). ICAM-1, intercellular adhesion molecule-1.

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.
7.
Fig. 1

Fig. 1. From: Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells.

Schematic drawing of an alveolus in state of early inflammation. Effector cell recruitment by inflammatory mediators from pulmonary epithelial and endothelial cells is illustrated (left side). Water transport through ion channels located on the alveolar epithelial cell apical surface and basolateral membrane (right side) is impaired. Sodium enters the cell via apical epithelial sodium channels (ENaC). On the basolateral interface, sodium is excreted via Na+/K+-ATPase, while potassium enters the cell. Reabsorption of sodium goes along with the reabsorption of Cl, which generates an osmotic driving force for the transepithelial movement of water. Radioactive marker ions (22Na+ for Na+ and 86Rb for K+) were used to measure the ion channel turnover. CINC-1, cytokine-induced neutrophil chemoattractant-1; MCP-1, monocyte chemoattractant protein-1; IL, interleukin.

M Urner, et al. Clin Exp Immunol. 2012 August;169(2):119-128.

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