Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling.

@article{Roman2006AdenosineIF,
  title={Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling.},
  author={Jesse Roman and Hilda N. Rivera and Susanne Roser-Page and Shanthi V. Sitaraman and Jeffrey D. Ritzenthaler},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2006},
  volume={290 2},
  pages={
          L317-25
        }
}
Adenosine is an extracellular nucleoside that is elevated in tissues during hypoxia and ischemia reperfusion and has been implicated in asthma and other lung disorders. There, adenosine is considered an important modulator of physiological functions and inflammation, but its effects on matrix expression and turnover during tissue remodeling are unknown. We examined the effects of adenosine on lung epithelial cells with particular attention to the expression of fibronectin, a matrix glycoprotein… 
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28 Citations
Background Citations
15
Methods Citations
2
Results Citations
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28 Citations

Citation Type

Citation Type

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TLDR
The crosstalk between P2Y(2)R- and EGFR-dependent signaling cascades converge to induce mediator release, whereas the latter also induces cytoskeletal rearrangement for cell migration and proliferation.
A2B Adenosine Receptors Induce IL-19 from Bronchial Epithelial Cells, Resulting in TNF-α Increase
TLDR
5′-(N-ethylcarboxamido)-adenosine (NECA), a stable analog of adenosine, increased the release of IL-19 by 4.6- ± 1.1-fold and a selective antagonist of the A2B receptor, CVT-6694, attenuated this effect of NECA.
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TLDR
This study demonstrates a novel mechanism by which extracellular adenosine modulates resistance to lung infection by targeting bacterial-host interactions and directly affects pneumococcal-epithelial cell interactions.
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The A2B Adenosine Receptor Modulates the Epithelial– Mesenchymal Transition through the Balance of cAMP/PKA and MAPK/ERK Pathway Activation in Human Epithelial Lung Cells
TLDR
For the first time the A2BAR has been related to the EMT process, and therefore to the different EMT-related pathologies, and its ability to affect different intracellular pathways could represent a mechanism at the basis of EMT maintenance/inhibition based on the extracellular microenvironment.
A1 adenosine receptor signaling reduces Streptococcus pneumoniae adherence to pulmonary epithelial cells by targeting expression of platelet‐activating factor receptor
TLDR
A novel mechanism by which extracellular adenosine modulates resistance to lung infection by targeting bacterial–host interactions is demonstrated by triggering A1 signaling boosted host resistance of old mice to S. pneumoniae pulmonary infection.
High-mobility group box 1 promotes extracellular matrix synthesis and wound repair in human bronchial epithelial cells.
TLDR
A role for HMGB1 is suggested in human airway epithelial cell repair and restitution via multiple pathways mediated by TLR4 and RAGE that underpin increased ECM synthesis and modulation of cell-matrix adhesion.
Inflammasome activators induce fibronectin expression and release in macrophages
TLDR
Results indicate that Fn plays a critical role in inflammasome‐activated cells by amplifying caspase‐1 activation and inducing inflammatory cell death.
Alterations in Adenosine Metabolism and Signaling in Patients with Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
TLDR
This study provides the first evidence that A2BR signaling can promote the production of inflammatory and fibrotic mediators in patients with these disorders.
Adenosine receptors and asthma.
TLDR
The roles of adenosine and AR subtypes in many of the characteristic features of asthma: airway obstruction, inflammation, bronchial hyperresponsiveness and remodeling are highlighted and the merit of targeting each receptor subtype in the development of novel antiasthma drugs is discussed.
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