title: Secondhand smoke exposure toxicity accelerates age-related cardiac disease in old hamsters.
abstract: BACKGROUND
  Aging is associated with physiological or pathological left ventricular hypertrophy (LVH) cardiac changes. Secondhand smoke (SHS) exposure is associated with pathological LVH. The action mechanism in cardiac concentric hypertrophy from SHS exposure is understood, but the transition contributed from SHS exposure is not. To determine whether exposure to SHS has an impact on age-induced LVH we examined young and old hamsters that underwent SHS exposure in a chamber for 30 mins.
  
  
  METHODS
  Morphological and histological studies were then conducted using hematoxylin and eosin (H&E) and Masson's trichrome staining. Echocardiographic analysis was used to determine left ventricular wall thickness and function. LVH related protein expression levels were detected by western blot analysis.
  
  
  RESULTS
  The results showed that both young and aged hamsters exposed to SHS exhibited increased heart weights and left ventricular weights, left ventricular posterior wall thickness and intraventricular septum systolic and diastolic pressure also increased. However, left ventricular function systolic and diastolic pressure deteriorated. H&E and Masson's trichrome staining results showed LV papillary muscles were ruptured, resulting in lower cardiac function at the myocardial level. LV muscle fiber arrangement was disordered and collagen accumulation occurred. Concentric LVH related protein molecular markers increased only in young hamsters exposed to SHS. However, this declined with hamster age. By contrast, eccentric LVH related proteins increased in aging hamsters exposed the SHS. Pro-inflammatory proteins, IL-6, TNF-α, JAK1, STAT3, and SIRTI expression increased in aging hamsters exposed to SHS.
  
  
  CONCLUSIONS
  We suggest that SHS exposure induces a pro-inflammatory response that results in concentric transition to aging eccentric LVH.
authors.forename: Jia-Ping
authors.initials: JP
authors.lastname: Wu
authors.forename: Cheng-Hong
authors.initials: CH
authors.lastname: Hsieh
authors.forename: Tsung-Jung
authors.initials: TJ
authors.lastname: Ho
authors.forename: Wei-Wen
authors.initials: WW
authors.lastname: Kuo
authors.forename: Yu-Lan
authors.initials: YL
authors.lastname: Yeh
authors.forename: Chien-Chung
authors.initials: CC
authors.lastname: Lin
authors.forename: Chia-Hua
authors.initials: CH
authors.lastname: Kuo
authors.affiliation: Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan. cyhuang@mail.cmu.edu.tw.
authors.forename: Chih-Yang
authors.initials: CY
authors.lastname: Huang
mesh_terms: D000367:Age Factors; D000818:Animals; D019703:Calcineurin / Q000378:metabolism; D006224:Cricetinae; D016207:Cytokines / Q000097:blood; D050991:GATA4 Transcription Factor / Q000378:metabolism; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology*; D020935:MAP Kinase Signaling System / Q000502:physiology; D050778:NFATC Transcription Factors / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D016207:Cytokines; D050991:GATA4 Transcription Factor; D050778:NFATC Transcription Factors; D014028:Tobacco Smoke Pollution; D019703:Calcineurin