title: Senescence marker protein-30 protects mice lungs from oxidative stress, aging, and smoking.
abstract: BACKGROUND
  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.
  
  
  OBJECTIVE
  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.
  
  
  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.
authors.affiliation: Department of Respiratory Medicine, Juntendo University, School of Medicine, Tokyo 113-8421, Japan. satotada@med.juntendo.ac.jp
authors.forename: Tadashi
authors.initials: T
authors.lastname: Sato
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Seyama
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Sato
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Mori
authors.forename: Sanae
authors.initials: S
authors.lastname: Souma
authors.forename: Taeko
authors.initials: T
authors.lastname: Akiyoshi
authors.forename: Yuzo
authors.initials: Y
authors.lastname: Kodama
authors.forename: Takanori
authors.initials: T
authors.lastname: Mori
authors.forename: Sataro
authors.initials: S
authors.lastname: Goto
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Takahashi
authors.forename: Yoshinosuke
authors.initials: Y
authors.lastname: Fukuchi
authors.forename: Naoki
authors.initials: N
authors.lastname: Maruyama
authors.forename: Akihito
authors.initials: A
authors.lastname: Ishigami
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001835:Body Weight; D002135:Calcium-Binding Proteins / Q000502:physiology*; D005978:Glutathione / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins; D008168:Lung / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D050050:Protein Carbonylation / Q000502:physiology*; D012907:Smoking / Q000009:adverse effects*; D015238:Sulfotransferases
chemical_list: D002135:Calcium-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; C513324:Rgn protein, mouse; D008315:Malondialdehyde; D015238:Sulfotransferases; C028152:alcohol sulfotransferase; D005978:Glutathione