Effect of aging on the expression of intracellular Ca2+ transport proteins in a rat heart
ABSTRACT Aging process is accompanied by various biological dysfunctions including altered calcium homeostasis. Modified calcium handling
might be responsible for changed cardiac function and potential development of the pathological state. In the present study
we compared the mRNA and protein levels of the intracellular Ca2+-handling proteins—inositol 1,4,5-trisphosphate receptor (IP3R), ryanodine receptor (RyR), sarcoplasmic reticulum Ca2+ pump (SERCA2), and also transient receptor potential C (TRPC) channels in cardiac tissues of 5-, 15-, and 26-month-old rats.
Aging was accompanied by significant increase in the mRNA levels of IP3R and TRPC channels in both ventricles and atria, but mRNA level of the type 2 RyR was unchanged. Protein content of the IP3R1 correlated with mRNA levels, in the left ventricle of 15- and 26-month-old rats the value was approximately 1.8 and 2.8-times
higher compared to 5-month-old rats. No significant differences were observed in mRNA and protein levels of the SERCA2 among
5-month-old and aged rats. However, Ca2+-ATPase activity significantly decreased with age, activities in 5-, 15-, and 26-month-old rats were 421.2±13.7, 335.5±18.1
and 304.6±14.8nmolPimin-1mg−1. These results suggest that altered transporting activity and/or gene expression of Ca2+-handling proteins of intracellular Ca2+ stores might affect cardiac function during aging.
Article: Cardioprotection and ageing.[show abstract] [hide abstract]
ABSTRACT: With an increase in the elderly population and an increase in the prevalence of age-related cardiovascular disease, anesthesiologists are increasingly being faced with elderly patients with known or suspected ischemic heart disease in the perioperative period. Although early reperfusion remains the best strategy to reduce ischemic injury, reperfusion may damage the myocardium. Adjuvant therapy to revascularization is therefore necessary. To develop better strategies to prevent ischemia-reperfusion injury in older patients, we need to understand the aged myocardium, which has undergone structural and functional changes relative to the normal myocardium, resulting in reduced functional capacity and vulnerability to ischemia-reperfusion injury. In addition, innate or acquired cardioprotection deteriorates with aging. These changes in the aged myocardium might explain why there is poor translation of basic research findings from young animals to older patients. In this review, I discuss changes in intracellular signaling associated with myocardial ageing that have an effect on ischemia-reperfusion injury, and I discuss the efficacy of cardioprotection afforded by ischemic and pharmacologic pre-and post-conditioning in the aged myocardium. Finally, I outline strategies to restore protection in the aged myocardium.Korean journal of anesthesiology 03/2010; 58(3):223-30.
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ABSTRACT: The tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca(2+) signaling is a key determinant of cellular health and cellular fate through the control of apoptosis and autophagy. Proteins that prevent or promote apoptosis and autophagy can affect intracellular Ca(2+) dynamics and homeostasis through binding and modulation of the intracellular Ca(2+)-release and Ca(2+)-uptake mechanisms. During aging, oxidative stress becomes an additional factor that affects ER and mitochondrial function and thus their role in Ca(2+) signaling. Importantly, mitochondrial dysfunction and sustained mitochondrial damage are likely to underlie part of the aging process. In this paper, we will discuss the different mechanisms that control intracellular Ca(2+) signaling with respect to apoptosis and autophagy and review how these processes are affected during aging through accumulation of reactive oxygen species.Journal of aging research 01/2011; 2011:920178.