Senescence marker protein-30 protects mice lungs from oxidative stress, aging, and smoking

Tadashi Sato, Kuniaki Seyama, Yasunori Sato, Hiroaki Mori, Sanae Souma, Taeko Akiyoshi, Yuzo Kodama, Takanori Mori, S. Goto, Kazuhisa Takahashi, Yoshinosuke Fukuchi, Naoki Maruyama, Akihito Ishigami

Research output: Contribution to journalArticle

127 Citations (Scopus)

Abstract

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 wk. 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-wk 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.

Original languageEnglish
Pages (from-to)530-537
Number of pages8
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume174
Issue number5
DOIs
Publication statusPublished - Sep 1 2006

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Oxidative Stress
Smoking
Lung
Smoke
Tobacco Products
Proteins
Pulmonary Emphysema
Malondialdehyde
Glutathione
Apoptosis
Mouse Rgn protein
Bronchoalveolar Lavage Fluid
Knockout Mice
Lung Diseases
Animal Models

Keywords

  • Aging
  • Oxidative stress
  • Pulmonary emphysema
  • Senescence marker protein-30
  • Smoking

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Senescence marker protein-30 protects mice lungs from oxidative stress, aging, and smoking. / Sato, Tadashi; Seyama, Kuniaki; Sato, Yasunori; Mori, Hiroaki; Souma, Sanae; Akiyoshi, Taeko; Kodama, Yuzo; Mori, Takanori; Goto, S.; Takahashi, Kazuhisa; Fukuchi, Yoshinosuke; Maruyama, Naoki; Ishigami, Akihito.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 174, No. 5, 01.09.2006, p. 530-537.

Research output: Contribution to journalArticle

Sato, T, Seyama, K, Sato, Y, Mori, H, Souma, S, Akiyoshi, T, Kodama, Y, Mori, T, Goto, S, Takahashi, K, Fukuchi, Y, Maruyama, N & Ishigami, A 2006, 'Senescence marker protein-30 protects mice lungs from oxidative stress, aging, and smoking', American Journal of Respiratory and Critical Care Medicine, vol. 174, no. 5, pp. 530-537. https://doi.org/10.1164/rccm.200511-1816OC
Sato, Tadashi ; Seyama, Kuniaki ; Sato, Yasunori ; Mori, Hiroaki ; Souma, Sanae ; Akiyoshi, Taeko ; Kodama, Yuzo ; Mori, Takanori ; Goto, S. ; Takahashi, Kazuhisa ; Fukuchi, Yoshinosuke ; Maruyama, Naoki ; Ishigami, Akihito. / Senescence marker protein-30 protects mice lungs from oxidative stress, aging, and smoking. In: American Journal of Respiratory and Critical Care Medicine. 2006 ; Vol. 174, No. 5. pp. 530-537.
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abstract = "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 wk. 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-wk 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.",
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AU - Akiyoshi, Taeko

AU - Kodama, Yuzo

AU - Mori, Takanori

AU - Goto, S.

AU - Takahashi, Kazuhisa

AU - Fukuchi, Yoshinosuke

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