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Published ahead of print on May 25, 2006, doi:10.1164/rccm.200511-1816OC

Am. J. Respir. Crit. Care Med., Volume 174, Number 5, September 2006, 530-537

A more recent version of this article appeared on September 1, 2006
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Submitted on November 28, 2005
Accepted on May 24, 2006

Senescence Marker Protein-30 Protects Mice Lungs from Oxidative Stress, Aging and Smoking

Tadashi Sato1*, Kuniaki Seyama2, Yasunori Sato3, Hiroaki Mori2, Sanae Souma2, Taeko Akiyoshi2, Yuzo Kodama2, Takanori Mori2, Sataro Goto4, Kazuhisa Takahashi2, Yoshinosuke Fukuchi2, Naoki Maruyama5, and Akihito Ishigami5

1 School of Medicine, Department of Respiratory Medicine, Juntendo University, Tokyo, Japan; Department of Molecular Pathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan, 2 School of Medicine, Department of Respiratory Medicine, Juntendo University, Tokyo, Japan, 3 Department of Molecular Pathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan; Faculty of Pharmaceutical Sciences, Department of Biochemistry, Toho University, Chiba, Japan, 4 Faculty of Pharmaceutical Sciences, Department of Biochemistry, Toho University, Chiba, Japan, 5 Department of Molecular Pathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: satotada{at}med.juntendo.ac.jp.

Rationale: Senescence marker protein-30 (SMP30) is a multifunctional protein providing protection to cellular functions from age-associated deterioration. We previously reported that SMP30 knockout (SMP30Y/-) mice are capable of being novel models for senile lung with age-related airspace enlargement and enhanced susceptibility to harmful stimuli. Objectives: Aging and smoking are considered as major contributing factors for the development of pulmonary emphysema. We evaluated whether SMP30Y/- mice are susceptible to oxidative stress associated with aging and smoking. Methods: Age-related changes of protein carbonyls in lung tissues from the wild-type (SMP30Y/+) and SMP30Y/- mice were evaluated. Both strains were exposed to cigarette smoke for 8 weeks and histopathologic and morphologic evaluations of the lungs, protein carbonyls and malondialdehyde in the lung tissues, total glutathione content in the bronchoalveolar lavage fluid, and degree of apoptosis of lung cells were determined. Measurements and Main Results: In the lungs of SMP30Y/- mice, protein carbonyls tended to increase with aging and were significantly higher than the age-matched SMP30Y/+ mice. Cigarette smoke exposure generated marked airspace enlargement (23.3% increase of the mean linear intercepts) with significant parenchymal destruction in the SMP30Y/- mice but not in the SMP30Y/+ mice (5.4%). The protein carbonyls, malondialdehyde, total glutathione, and apoptosis of lung cells were significantly increased after 8-week exposure to cigarette smoke in the SMP30Y/- mice. Conclusions: Our results suggest that SMP30 protects mice lungs from oxidative stress associated with aging and smoking. The SMP30Y/- mice could be useful animal models for investigating age-related lung diseases including cigarette smoke-induced pulmonary emphysema.
Key words: senescence marker protein-30, oxidative stress, aging, smoking, pulmonary emphysema




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