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Published ahead of print on August 27, 2004, doi:10.1165/rcmb.2003-0290OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 6, December 2004, 643-649

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Submitted on August 5, 2003
Revised on August 26, 2004

CIGARETTE SMOKE INDUCES SENESCENCE IN ALVEOLAR EPITHELIAL CELLS

Takao Tsuji1, Kazutetsu Aoshiba1*, and Atsushi Nagai1

1 First Department of Medicine, Tokyo Women's Medical University, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: kaoshiba{at}chi.twmu.ac.jp.

Cellular senescence is a state of irreversible growth arrest induced either by telomere shortening (replicative senescence) or by telomere-independent signals (stress-induced senescence). The alveolar epithelium is often injured by a variety of inhaled toxins, including cigarette smoke (CS). In the present study, we investigated whether exposure to CS induces senescence of alveolar epithelial cells. In vitro experiments showed that exposure of A549 cells or normal human alveolar epithelial cells to sublethal concentrations of aqueous CS extracts (CSE) induced cellular senescence. The senescence was characterized by a dose- and time-dependent increase in senescence-associated b-galactosidase (SA-{beta}-gal) activity, senescence-associated changes in cell morphology, an increase in cell size and lysosomal mass, accumulation of lipofuscin, overexpression of p21CIP1/WAF1/Sdi1 protein, and irreversible growth arrest. In vivo experiments in ICR mice showed that inhalation of CS for 2 weeks induced increases in SA-{beta}-gal activity, lipofuscin accumulation, and p21CIP1/WAF1/Sdi1 protein expression in alveolar epithelial cells. These results suggest that CS induces a phenotype that is indistinguishable from that of senescence in alveolar epithelial cells. The induction of cellular senescence by CS may contribute to impaired reepithelialization leading to CS-related chronic lung diseases.




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