Subcellular [Ca 2 (cid:49) ] i Gradients During Excitation-Contraction Coupling in Newborn Rabbit Ventricular Myocytes
Subcellular [Ca 2 (cid:49) ] i Gradients During Excitation-Contraction Coupling in Newborn Rabbit Ventricular Myocytes
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新生兔心室肌细胞兴奋-收缩耦合过程中的亚细胞 [Ca 2 (cid:49) ] i 梯度
DOI：
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发表时间：
1999
期刊：
影响因子：
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通讯作者：
M. Artman
中科院分区：
文献类型：
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作者：
P. Haddock;W. Coetzee;Emily Cho;L. Porter;H. Katoh;D. Bers;M. S. Jafri;M. Artman
- 在成人（AD）心室肌细胞中，T-小管和肌浆网（SR）二向连接在兴奋-收缩（EC）偶联中的中心作用表明，它们在新生（NB）细胞中的缺失可能表现为改变的EC偶联表型。我们使用共聚焦显微镜比较场刺激NB和AD兔心室肌细胞的肌膜下空间和细胞中心的fluo-3 [Ca 2（cid：49）] i瞬变。收缩期峰值[Ca 2（cid：49）] i出现早，肌膜下高于细胞中心。在AD心肌细胞中，[Ca 2（cid：49）] i在细胞中心和肌膜下呈相似的变化趋势。抑制SR（10 mol/L毒胡萝卜素）可减慢AD心肌细胞Ca 2（cid：49）的升降速率，但不改变NB心肌细胞Ca 2（cid：49）的瞬时动力学。与成人相比，局部SR Ca 2（cid：49）释放事件（“Ca 2（cid：49）火花”）主要发生在NB肌细胞的细胞周边。免疫标记实验显示AD心肌细胞中Na（cid：49）-Ca 2（cid：49）交换体和Ryanodine受体（RyR 2）的重叠分布。相反，RyR 2在空间上与NB肌细胞的肌膜分离。di-8-ANEPPS处理的肌细胞的共聚焦肌膜成像证实了AD细胞中广泛的T-小管网络，并且NB肌细胞中不存在T-小管。亚细胞Ca 2（cid：49）动力学的数学模型预测，在动作电位过程中通过Na（cid：49）-Ca 2（cid：49）交换器的Ca 2（cid：49）通量可以解释NB肌细胞中肌膜下Ca 2（cid：49）梯度。肌膜Ca 2（cid：49）进入与SR Ca 2（cid：49）释放通道的空间分离可能使正常EC偶联过程中SR Ca 2（cid：49）释放的作用最小化。瑟克水库1999;85：415-427）。
—The central role of T-tubule and sarcoplasmic reticulum (SR) diadic junctions in excitation-contraction (EC) coupling in adult (AD) ventricular myocytes suggests that their absence in newborn (NB) cells may manifest as an altered EC coupling phenotype. We used confocal microscopy to compare fluo-3 [Ca 2 (cid:49) ] i transients in the subsarcolemmal space and cell center of field-stimulated NB and AD rabbit ventricular myocytes. Peak systolic [Ca 2 (cid:49) ] i occurred sooner and was higher in the subsarcolemmal space compared with the cell center in NB myocytes. In AD myocytes, [Ca 2 (cid:49) ] i rose and declined with similar profiles at the cell center and subsarcolemmal space. Disabling the SR (10 (cid:109) mol/L thapsigargin) slowed the rate of rise and decline of Ca 2 (cid:49) in AD myocytes but did not alter Ca 2 (cid:49) transient kinetics in NB myocytes. In contrast to adults, localized SR Ca 2 (cid:49) release events (“Ca 2 (cid:49) sparks”) occurred predominantly at the cell periphery of NB myocytes. Immunolabeling experiments demonstrated overlapping distributions of the Na (cid:49) -Ca 2 (cid:49) exchanger and ryanodine receptors (RyR2) in AD myocytes. In contrast, RyR2s were spatially separated from the sarcolemma in NB myocytes. Confocal sarcolemmal imaging of di-8-ANEPPS–treated myocytes confirmed an extensive T-tubule network in AD cells, and that T-tubules are absent in NB myocytes. A mathematical model of subcellular Ca 2 (cid:49) dynamics predicts that Ca 2 (cid:49) flux via the Na (cid:49) -Ca 2 (cid:49) exchanger during an action potential can account for the subsarcolemmal Ca 2 (cid:49) gradients in NB myocytes. Spatial separation of sarcolemmal Ca 2 (cid:49) entry from SR Ca 2 (cid:49) release channels may minimize the role of SR Ca 2 (cid:49) release during normal EC coupling in NB ventricular myocytes. Circ Res . 1999;85:415-427.)
影响因子：
56.9
作者：
ALLBRITTON, NL;MEYER, T;STRYER, L
通讯作者：
STRYER, L
影响因子：
3.4
作者：
CANNELL, MB;CHENG, H;LEDERER, WJ
通讯作者：
LEDERER, WJ
影响因子：
3.8
作者：
Keizer, J;Smith, GD
通讯作者：
Smith, GD