ArticleToxicology letters2008
Acute damage by naphthalene triggers expression of the neuroendocrine marker PGP9.5 in airway epithelial cells.
Article in Toxicology letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- NOTCH1 is required for regeneration of Clara cells during repair of airway injury.Stem cells (Dayton, Ohio) · 2012Article
- Achaete-scute homologue-1 tapers neuroendocrine cell differentiation in lungs after exposure to naphthalene.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Cell type-specific expression of adenomatous polyposis coli in lung development, injury, and repair.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Article
- Targeted cytosine deaminase-uracil phosphoribosyl transferase suicide gene therapy induces small cell lung cancer-specific cytotoxicity and tumor growth delay.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Article
- Signaling via Alk5 controls the ontogeny of lung Clara cells.Development (Cambridge, England) · 2010Article
- Stabilized beta-catenin in lung epithelial cells changes cell fate and leads to tracheal and bronchial polyposis.Developmental biology · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Protein Gene Product 9.5 (PGP9.5) is highly expressed in nervous tissue. Recently PGP9.5 expression has been found to be upregulated in the pulmonary epithelium of smokers and in non-small cell lung cancer, suggesting that it also plays a role in carcinogen-inflicted lung epithelial injury and carcinogenesis. We investigated the expression of PGP9.5 in mice in response to two prominent carcinogens found in tobacco smoke: Naphthalene and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). By immunostaining, we found that PGP9.5 protein was highly expressed throughout the airway epithelium in the days immediately following a single injection of naphthalene. In contrast, PGP9.5 was exclusively confined to neurons and neuroendocrine cells in the control and NNK-exposed lungs. Furthermore, we investigated the expression of PGP9.5 mRNA in the lungs by quantitative RT-PCR (qPCR). PGP9.5 mRNA expression was highly upregulated in the days immediately following naphthalene injection and gradually returning to that of control mice 5 days after naphthalene injection. In contrast, exposure to NNK did not result in a significant increase in PGP9.5 mRNA 10 weeks after exposure. No increased expression of two other neuroendocrine markers was found in the non-neuroendocrine epithelial cells after naphthalene exposure. In contrast, immunostaining for the cell cycle regulator p27(Kip1), which has previously been associated with PGP9.5 in lung cancer cells, revealed transient downregulation of p27(Kip1) in naphthalene exposed airways compared to controls, indicating that the rise in PGP9.5 in the airway epithelium is related to downregulation of p27(Kip1). This study is the first to specifically identify the carcinogen naphthalene as an inducer of PGP9.5 expression in non-neuroendocrine epithelium after acute lung injury and further strengthens the accumulating evidence of PGP9.5 as a central player in lung epithelial damage and early carcinogenesis.
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