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

Kaplán, Peter; Jurkovičová, Dana; Babušíková, Eva; Hudecová, Soňa; Račay, Peter; Sirova, Marta; Lehotský, Ján; Drgová, A; Dobrota, Dušan; Križanová, Oľga

doi:10.1007/s11010-007-9414-9

Cited by 44 publications

(28 citation statements)

References 36 publications

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“…SERCA 2a activity was determined from the rate of inorganic phosphate release, as described previously (18). The Ca 2ϩ -ATPase activity was calculated as the difference between Ca 2ϩ , Mg 2ϩ -ATPase activity (in the presence of calcium) and Mg 2ϩ -ATPase activity measured in the absence of calcium (3 mM EGTA).…”

Section: Methodsmentioning

confidence: 99%

The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension

Dupont

Maizel

Mentaverri

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Dupont S, Maizel J, Mentaverri R, Chillon JM, Six I, Giummelly P, Brazier M, Choukroun G, Tribouilloy C, Massy ZA, Slama M. The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension. Am J Physiol Heart Circ Physiol 302: H1524 -H1532, 2012. First published January 27, 2012; doi:10.1152/ajpheart.00955.2010.-Left ventricular (LV) diastolic dysfunction, particularly relaxation abnormalities, are known to be associated with the development of LV hypertrophy (LVH). Preliminary human and animal studies suggested that early LV diastolic dysfunction may be revealed independently of LVH. However, whether LV diastolic dysfunction is compromised before the onset of hypertension and LVH remains unknown. We therefore evaluated LV diastolic function in spontaneously hypertensive rats (SHR) at different ages and tested whether LV diastolic dysfunction is associated with abnormal intracellular calcium homeostasis. LV systolic and diastolic functions were evaluated by invasive and echocardiographic methods in 3-week-old (without hypertension) and 5-week-old (with hypertension) SHR and Wistar-Kyoto control rats. Basal intracytoplasmic calcium and sarcoplasmic reticulum (SR) Ca 2ϩ contents were measured in cardiomyocytes using fura-2 AM. Sarco(endo)plasmic Ca 2ϩ -ATPase isoform 2a (SERCA 2a) and phospholamban (PLB) expressions were quantified by Western blot and quantitative RT-PCR techniques. LV relaxation dysfunction was observed in 3-week-old SHR rats before onset of hypertension and LVH. An increase in basal intracytoplasmic Ca 2ϩ and a decrease in SR Ca 2ϩ release were demonstrated in SHR. Decreased expression of SERCA 2a and Ser16 PLB (p16-PLB) protein levels was also observed in SHR rats, whereas mRNA expression was not decreased. For the first time, we have shown that LV myocardial dysfunction precedes hypertension in 3-week-old SHR rats. This LV myocardial dysfunction was associated with high diastolic [Ca 2ϩ ]i possibly due to decreased SERCA 2a and p16-PLB protein levels. Diastolic dysfunction may be a potential predictive marker of arterial hypertension in genetic hypertension syndromes.diastole; ultrasonic; calcium; spontaneously hypertensive rats LEFT VENTRICULAR (LV) DIASTOLIC dysfunction is responsible for more than one half of all hospitalizations for congestive heart failure or acute pulmonary oedema, which has been shown to be the consequence of multiple clinical factors, mostly hypertension (15). LV diastolic dysfunction, particularly relaxation abnormalities, is usually recognized to be closely associated with the development of left ventricular hypertrophy (LVH) in hypertensive humans and spontaneously hypertensive rats (SHR), a model of human genetic hypertension (35). Nevertheless, in a previous study, we demonstrated LV relaxation impairment in young SHR without LVH (37), subsequently confirmed by Aeschbacher et al (1). Di Bello et al. (13) have also demonstrated early LV diastolic dysfunction before the onset of hypertension and LVH. In view of these da...

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Section: Methodsmentioning

confidence: 99%

The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension

Dupont

Maizel

Mentaverri

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…Its incidence increases with age, as does the expression of the IP 3 R in the heart [168]. Expression of the IP 3 R is augmented in a dog model of AF and in human AF [15,169,170].…”

Section: Atrial Fibrillationmentioning

confidence: 99%

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

Kockskämper

Zima

Roderick

et al. 2008

Journal of Molecular and Cellular Cardiology

168

149

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Inositol 1,4,5-trisphosphate (IP 3 ) is a ubiquitous intracellular messenger regulating diverse functions in almost all mammalian cell types. It is generated by membrane receptors that couple to phospholipase C (PLC), an enzyme which liberates IP 3 from phosphatidylinositol 4,5-bisphosphate (PIP 2 ). The major action of IP 3 , which is hydrophilic and thus translocates from the membrane into the cytoplasm, is to induce Ca 2+ release from endogenous stores through IP 3 receptors (IP 3 Rs). Cardiac excitation-contraction coupling relies largely on ryanodine receptor (RyR)-induced Ca 2+ release from the sarcoplasmic reticulum. Myocytes express a significantly larger number of RyRs compared to IP 3 Rs (∼100:1), and furthermore they experience substantial fluxes of Ca 2+ with each heartbeat. Therefore, the role of IP 3 and IP 3 -mediated Ca 2+ signaling in cardiac myocytes has long been enigmatic. Recent evidence, however, indicates that despite their paucity cardiac IP 3 Rs may play crucial roles in regulating diverse cardiac functions. Strategic localization of IP 3 Rs in cytoplasmic compartments and the nucleus enables them to participate in subsarcolemmal, bulk cytoplasmic and nuclear Ca 2+ signaling in embryonic stem cell-derived and neonatal cardiomyocytes, and in adult cardiac myocytes from the atria and ventricles. Intriguingly, expression of both IP 3 Rs and membrane receptors that couple to PLC/IP 3 signaling is altered in cardiac disease such as atrial fibrillation or heart failure, suggesting the involvement of IP 3 signaling in the pathology of these diseases. Thus, IP 3 exerts important physiological and pathological functions in the heart, ranging from the regulation of pacemaking, excitation-contraction and excitation-transcription coupling to the initiation and/or progression of arrhythmias, hypertrophy and heart failure. KeywordsInositol 1,4,5-trisphosphate; Cardiac myocyte; Calcium; Inotropy; Arrhythmias; Nucleus; Hypertrophy © 2008 Elsevier Inc. All rights reserved. * Corresponding author. E-mail address: jens.kockskaemper@meduni-graz.at (J. Kockskämper).. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript The discovery of IP 3A quarter of a century ago it was shown that D-myo inositol 1,4,5-trisphosphate (IP 3 ) releases Ca 2+ from a non-mitochondrial internal Ca 2+ store [1]. Since this hallmark discovery, IP 3 has emerged as a ubiquitous intracellular messenger, releasing Ca 2+ from stores through activation of IP 3 receptors (IP 3 Rs) in almost all eukaryotic cells. The major IP 3 -sensitive intracellular Ca 2+ store is the endoplasmic reticulum. However, IP 3 has also been shown to release Ca 2+ stored in other compartments, such as the Golgi and the nuclear envelope [2]. In addition, IP 3 Rs are present on the plasma membrane of some cell types, where they can gate Ca 2+ influx [3]. A crucial role for IP 3 -dependent Ca 2+ release has been demonstrated in many mammalian cell types, ranging from tiny platelets, where it initiates blood clottin...

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“…-ATPase [19]. It is known that Na + / K + -ATPase has three isoforms of catalytic (α) subunit having different affinities to cardiac glycoside ouabain: α 1 (low affinity), α 2 (middle affinity) and α 3 (high affinity).…”

Section: Introductionmentioning

confidence: 99%

Age-Dependent Brain Tissue Hydration, Ca Exchange and their Dose- Dependent Ouabain Sensitivity

Ayrapetyan¹

2012

JBB

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

Cited by 44 publications

References 36 publications

The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension

The onset of left ventricular diastolic dysfunction in SHR rats is not related to hypertrophy or hypertension

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

Age-Dependent Brain Tissue Hydration, Ca Exchange and their Dose- Dependent Ouabain Sensitivity

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