Secondhand Smoke Exposure Reduced the Compensatory Effects of IGF-I Growth Signaling in the Aging Rat Hearts

Int J Med Sci. 2015 Aug 28;12(9):708-18. doi: 10.7150/ijms.12032. eCollection 2015.

Abstract

Background: Secondhand smoke (SHS) exposure is associated with increased risk of cardiovascular disease. Aging is a physiological process that involves progressive impairment of normal heart functions due to increased vulnerability to damage. This study examines secondhand smoke exposure in aging rats to determine the age-related death-survival balance.

Methods: Rats were placed into a SHS exposure chamber and exposed to smog. Old age male Sprague-Dawley rats were exposed to 10 cigarettes for 30 min, day and night, continuing for one week. After 4 weeks the rats underwent morphological and functional studies. Left ventricular sections were stained with hematoxylin-eosin for histopathological examination. TUNEL detected apoptosis cells and protein expression related death and survival pathway were analyzed using western blot.

Results: Death receptor-dependent apoptosis upregulation pathways and the mitochondria apoptosis proteins were apparent in young SHS exposure and old age rats. These biological markers were enhanced in aging SHS-exposed rats. The survival pathway was found to exhibit compensation only in young SHS-exposed rats, but not in the aging rats. Further decrease in the activity of this pathway was observed in aging SHS-exposed rats. TUNEL apoptotic positive cells were increased in young SHS-exposed rats, and in aging rats with or without SHS-exposure.

Conclusions: Aging reduces IGF-I compensated signaling with accelerated cardiac apoptotic effects from second-hand smoke.

Keywords: Secondhand smoke exposure; age-related death-survival balance; aging; apoptosis.; cell cycle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / drug effects*
  • Aging / physiology
  • Animals
  • Apoptosis / drug effects
  • Caspase 8 / metabolism
  • Fas Ligand Protein / metabolism
  • Fas-Associated Death Domain Protein / metabolism
  • Heart / drug effects*
  • Inflammation / metabolism
  • Insulin-Like Growth Factor I / metabolism*
  • Male
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats, Sprague-Dawley
  • Signal Transduction
  • Tobacco Smoke Pollution / adverse effects*
  • Tumor Necrosis Factor-alpha / metabolism
  • Ventricular Remodeling / drug effects
  • fas Receptor / metabolism

Substances

  • Fadd protein, rat
  • Fas Ligand Protein
  • Fas protein, rat
  • Fas-Associated Death Domain Protein
  • Faslg protein, rat
  • Tobacco Smoke Pollution
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • Insulin-Like Growth Factor I
  • Proto-Oncogene Proteins c-akt
  • Caspase 8