A new rat type I-like alveolar epithelial cell line R3/1: bleomycin effects on caveolin expression

Koslowski, Roland; Barth, Kathrin; Augstein, Antje; Tschernig, Thomas; Bargsten, Gerhard; Aufderheide, Michaela; Kasper, Michael

doi:10.1007/s00418-004-0662-4

Cited by 55 publications

(45 citation statements)

References 52 publications

(51 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both cell lines have properties similar to those of AEC I (Kathuria et al, 2007;Koslowski et al, 2004). We confirmed that E10 cells had a very high expression of P2X 7 R and that R3/1 cells expressed little P2X 7 R (Fig.…”

Section: Bzatp Stimulates Surfactant Secretion In a Heterocellular Cusupporting

confidence: 77%

“…Another line of evidence favoring P2X 7 R as a mediator for the increase in surfactant secretion comes from co-culture of P2X 7 Rexpressing cells with AEC II. Two lung cell lines, E10 and R3/1, have AEC-I-like properties (Kathuria et al, 2007;Koslowski et al, 2004). However, E10 cells express a high level of P2X 7 R, whereas R3/1 cells have little P2X 7 R (Barth et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Purinergic P2X7 receptor regulates lung surfactant secretion in a paracrine manner

Mishra

Chintagari

Guo

et al. 2011

Journal of Cell Science

View full text Add to dashboard Cite

SummaryAlveolar epithelium is composed of alveolar epithelial cells of type I (AEC I) and type II (AEC II). AEC II secrete lung surfactant by means of exocytosis. P2X 7 receptor (P2X 7 R), a P2 purinergic receptor, has been implicated in the regulation of synaptic transmission and inflammation. Here, we report that P2X 7 R, which is expressed in AEC I but not AEC II, is a novel mediator for the paracrine regulation of surfactant secretion in AEC II. In primary co-cultures of AEC I and AEC II benzoyl ATP (BzATP; an agonist of P2X 7 R) increased surfactant secretion, which was blocked by the P2X 7 R antagonist Brilliant Blue G. This effect was observed in AEC II cocultured with human embryonic kidney HEK-293 cells stably expressing rat P2X 7 R, but not when co-cultured with AEC I in which P2X 7 R was knocked down or in co-cultures of AEC I and AEC II isolated from P2X 7 R -/-mice. BzATP-mediated secretion involved P2Y 2 receptor signaling because it was reduced by the addition of the ATP scavengers apyrase and adenosine deaminase and the P2Y 2 receptor antagonist suramin. However, the stimulation with BzATP might also release other substances that potentially increase surfactant secretion as a greater stimulation of secretion was observed in AEC II incubated with BzATP when co-cultured with E10 or HEK-293-P2X 7 R cells than with ATP alone. P2X 7 R -/-mice failed to increase surfactant secretion in response to hyperventilation, pointing to the physiological relevance of P2X 7 R in maintaining surfactant homeostasis in the lung. These results suggest that the activation of P2X 7 R increases surfactant secretion by releasing ATP from AEC I and subsequently stimulating P2Y 2 receptors in AEC II.

show abstract

Section: Bzatp Stimulates Surfactant Secretion In a Heterocellular Cusupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Purinergic P2X7 receptor regulates lung surfactant secretion in a paracrine manner

Mishra

Chintagari

Guo

et al. 2011

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…As confirmed by immunofluorescence analysis (Fig. I), R3/1 cells have been characterized as an adequate model to study in vitro AT-I cells and express RAGE and RTI40/TI-alpha, two well-characterized markers for AT-I cells, on cell surface (16,(19)(20)(21).…”

Section: Discussionmentioning

confidence: 72%

S100B Induces the Release of Pro-Inflammatory Cytokines in Alveolar Type I-like Cells

Piazza

Leggiero

Benedictis

et al. 2013

Int J Immunopathol Pharmacol

View full text Add to dashboard Cite

S100B, a 21kDa cytosolic calcium-binding protein of the EF-hand type, present in high abundance in the brain, stimulates inflammatory responses in different cellular types inside and outside the central nervous system. Most of extracellular S100B effects are mediated by Receptor for Advanced Glycation End-products (RAGE). RAGE is highly expressed in lung by Alveolar Type-I (AT-I) cells and its activation contributes to ALI/ARDS pathogenesis. In this in-vitro study, we tested the hypothesis that S100B (0.002μg/L, 0.02μg/L, 0.5μg/L, 5μg/L) stimulates an ATI-derived cell line (R3/1) to secrete inflammatory mediators involved in lung inflammation. Our main result is that S100B stimulates R3/1 cells to secrete TNF-alpha and IL-6 (well-known pro-inflammatory cytokines in lung inflammation and neurogenic pulmonary edema), but not sICAM-1, CINC-1 or CINC-3. Soluble RAGE (sRAGE) reduced SlOOB-dependent secretion of TNF-alpha but did not decrease S100B-dependent secretion of IL-6. Moreover, in absence of S100B, sRAGE enhanced IL-6 release. This study demonstrates that in vitro S100B dose-dependently stimulated R3/1 cells, to enhance the secretion of TNF-alpha and IL-6; S100B pro-inflammatory activity might be mediated at least in part by RAGE. Besides acting as decoy receptor, sRAGE could have pro-inflammatory properties.

show abstract

“…12 Nonetheless, although Cav-2 is highly expressed in the lungs, investigation of its role in lung fibrosis is still neglected.…”

Section: Report Reportmentioning

confidence: 99%

Genetic ablation of caveolin-2 sensitizes mice to bleomycin-induced injury

Almeida

Jasmin²,

Galdo³

et al. 2013

Cell Cycle

View full text Add to dashboard Cite

A new rat type I-like alveolar epithelial cell line R3/1: bleomycin effects on caveolin expression

Cited by 55 publications

References 52 publications

Purinergic P2X7 receptor regulates lung surfactant secretion in a paracrine manner

Purinergic P2X7 receptor regulates lung surfactant secretion in a paracrine manner

S100B Induces the Release of Pro-Inflammatory Cytokines in Alveolar Type I-like Cells

Genetic ablation of caveolin-2 sensitizes mice to bleomycin-induced injury

Contact Info

Product

Resources

About