Anti-tissue remodeling effects of corticosteroids: fluticasone propionate inhibits fibronectin expression in fibroblasts.

@article{Tomic2005AntitissueRE,
  title={Anti-tissue remodeling effects of corticosteroids: fluticasone propionate inhibits fibronectin expression in fibroblasts.},
  author={Rade Tomic and Charles C Lassiter and Jeffrey D. Ritzenthaler and Hilda N. Rivera and Jesse Roman},
  journal={Chest},
  year={2005},
  volume={127 1},
  pages={
          257-65
        }
}
OBJECTIVES Tissue remodeling often accompanies diseases such as COPD that are caused by or aggravated by tobacco exposure. Inhaled or systemic corticosteroids are frequently used for the treatment of these illnesses, and their beneficial effects are often ascribed to their anti-inflammatory properties. However, their role in tissue remodeling remains unclear. This study was designed to evaluate the role of corticosteroids in matrix expression in vitro. DESIGN We investigated the effects of… 
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30 Citations
Background Citations
10
Methods Citations
8

30 Citations

Citation Type

Citation Type

A phosphodiesterase 4 inhibitor inhibits matrix protein deposition in airways in vitro.
Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling.
TLDR
Overall, the observations suggest that adenosine might modulate tissue remodeling by stimulating fibronectin expression in lung epithelial cells through induction of purinergic receptor-mediated signals that target CREB phosphorylation and stimulate fibronECTin gene transcription.
Increased fibronectin expression in lung in the setting of chronic alcohol abuse.
TLDR
Alveolar macrophages from subjects with alcohol abuse demonstrated increased fibronectin mRNA expression, and their ELF also elicited more fibronsectin gene transcription in lung fibroblasts compared with controls, suggesting activation of tissue remodeling that may contribute to the increased susceptibility for the ARDS observed in alcoholism.
Bronchial vascular remodelling in patients with COPD and its relationship with inhaled steroid treatment
TLDR
Bronchial vascular remodelling in patients with COPD is mainly related to morphological changes of the mucosal microvessels rather than to new vessel formation, and may be reduced in patients treated with steroids.
Ethanol stimulates the expression of fibronectin in lung fibroblasts via kinase-dependent signals that activate CREB.
TLDR
Observations suggest that ethanol or ethanol metabolites stimulate lung fibroblasts to produce fibronectin by inducing specific signals transmitted via nAChRs independent of the alpha(7-)subunit, and this might represent a mechanism by which ethanol renders the lung susceptible to acute lung injury.
The effect of asthma therapeutics on signalling and transcriptional regulation of airway smooth muscle function.
The extracellular matrix – the under‐recognized element in lung disease?
TLDR
Emerging data suggest that alterations in the composition, folding or rigidity of ECM proteins may alter the functional responses of cells within their environs, and in so doing change the pathological outcomes.
Opposite effect of fluticasone and salmeterol on fibronectin and tenascin‐C expression in primary human lung fibroblasts
TLDR
Current therapies for asthma and COPD consist of inhaled corticosteroids and long‐acting β2‐agonists (LABA), however, their effect on airway remodelling is not well understood so far.
Epithelial-derived Fibronectin Expression, Signaling, and Function in Intestinal Inflammation*
TLDR
The data show that epithelial-derived FN potentiates cell attachment and wound healing through epithelium-matrix interactions and that FN expression may have important implications for maintaining normal epithelial integrity as well as regulating epithelial response to injury during colitis.
Nicotinic acetylcholine receptors are sensors for ethanol in lung fibroblasts.
TLDR
It is suggested that α4 nA ChRs serve as sensors for EtOH-induced oxidant stress in lung fibroblasts, thereby revealing a new mechanism by which EtOH may affect lung cells and tissue remodeling and pointing to nAChRs as potential targets for intervention.
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