Effect of aging on the expression of intracellular Ca²⁺ transport proteins in a rat heart

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...

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Veröffentlicht in:Molecular and cellular biochemistry 2007-07, Vol.301 (1-2), p.219-226
Hauptverfasser: Kaplan, P, Jurkovicova, D, Babusikova, E, Hudecova, S, Racay, P, Sirova, M, Lehotsky, J, Drgova, A, Dobrota, D, Krizanova, O
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Sprache:eng
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Zusammenfassung: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 ± 14.8 nmol Pi min⁻¹ mg-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.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-007-9414-9