Cigarette smoke induces cyclooxygenase-2 and microsomal prostaglandin E2 synthase in human lung fibroblasts: implications for lung inflammation and cancer.

@article{Martey2004CigaretteSI,
  title={Cigarette smoke induces cyclooxygenase-2 and microsomal prostaglandin E2 synthase in human lung fibroblasts: implications for lung inflammation and cancer.},
  author={Christine A Martey and Stephen J. Pollock and Chantal K Turner and Katherine O'Reilly and Carolyn J. Baglole and Richard P. Phipps and Patricia J. Sime},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2004},
  volume={287 5},
  pages={
          L981-91
        }
}
  • C. A. Martey, S. Pollock, P. Sime
  • Published 1 November 2004
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
Cigarette smoking can lead to many human pathologies including cardiovascular and respiratory disease. Recent studies have defined a role for fibroblasts in the development of colon cancer. Moreover, fibroblasts are now thought of as key "sentinel" cells that initiate inflammation by releasing proinflammatory mediators including prostaglandins (PGs). Pathological overexpression of cyclooxygenase-2 (COX-2) and excess eicosanoid production are found in the early stages of carcinogenesis. By… 
The aryl hydrocarbon receptor is a regulator of cigarette smoke induction of the cyclooxygenase and prostaglandin pathways in human lung fibroblasts.
TLDR
The central role of the aryl hydrocarbon receptor (AHR) in cigarette smoke extract (CSE)-induced COX-2, microsomal PGE(2) synthase (mPGES), and PGE (2) production in human lung fibroblasts is reported.
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It is suggested that CSE promote the induction of COX-2 and contributes to the proinflammatory effects of PGE(2) in the airways of COPD subjects.
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PGE2 is a critical component of an amplifying and self-perpetuating circle inducing senescence and inflammation in COPD fibroblasts and Modulating the described PGE2 signaling pathway could provide a new basis to dampen senescENCE and senescences-associated inflammation in CopD.
Microsomal Prostaglandin E Synthase-1 in Respiratory Diseases
TLDR
The most recent advances in the understanding of mPGES-1 in airway inflammation, COPD, allergic airway diseases, respiratory response to hypoxia, and lung cancers are covered.
Cigarette smoke induces proinflammatory cytokine release by activation of NF-kappaB and posttranslational modifications of histone deacetylase in macrophages.
TLDR
Cigarette smoke-induced release of IL-8 is associated with activation of NF-kappaB via IKK and reduction in HDAC levels/activity in macrophages and inhibition of IKK ablated the CSE-mediatedIL-8 release.
Pathway to Elevate Cyclooxygenase 2 Expression and Prostaglandin E 2 Secretion in Human Bronchial Epithelial Cells
TLDR
It is suggested that E2 enhanced OHE2-increased intracellular oxidative stress which increased NF-kB activity, COX-2 expression, and PGE2 secretion, and the present data suggest a pathway that contributes an epigenetic mechanism to the overall mechanism of carcinogenesis.
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