Steady-state coupling of plasma membrane calcium entry to extrusion revealed by novel L-type calcium channel block.
Steady-state coupling of plasma membrane calcium entry to extrusion revealed by novel L-type calcium channel block.
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DOI：
10.1016/j.ceca.2008.01.004
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发表时间：
2008-10
期刊：
影响因子：
4
通讯作者：
Satin, Jonathan
中科院分区：
文献类型：
--
作者：
Lester, William C.;Schroder, Elizabeth A.;Burgess, Don E.;Yozwiak, Doug;Andres, Douglas A.;Satin, Jonathan
The L-type Ca2+ channel (CaV1.2) is the main pathway for trans-sarcolemmal (SL) Ca2+ influx in cardiac myocytes. To maintain Ca2+ homeostasis, chronic SL Ca2+-influx must be matched by chronic SL efflux. In this study we tested the hypothesis that chronic down-regulation of SL Ca2+-entry regulates SL extrusion. We studied mRNA and Ca2+ handling responses to chronic down-regulation of Ca2+ channel current induced by over-expression of the small GTPase Rem. Rem lowered net SL diastolic Ca2+-entry, and reduced the twitch Ca2+ amplitude. Rem also significantly slowed Ca2+ transient decay kinetics (p<10-3). Rem reduced NCX1.1 protein level and function. To measure Na-Ca2+-exchange (NCX) function and sarcoplasmic reticulum (SR) store load we perfused Ca2+-free bath for 25s followed by rapid application of 50mM caffeine. In control, caffeine transient relaxations were described by a bi-exponential decay with a fast phase that was 10mM Ni2+-senstive. Rem significantly slowed caffeine-induced relaxation time course (Rem vs control, p<10-6). To test whether extrusion slowing was mediated by insufficient basal Ca2+ for allosteric NCX activation we measured the effect of increasing bath Ca2+ from 1.8 to 6mM on caffeine-induced relaxation kinetics. 6mM Ca2+ did not alter kinetics of control cells, but in Rem-over-expressed cells 6mM Ca2+ sped kinetics. We conclude that chronic block of CaV1.2 channel-mediated SL entry alters NCX expression, and coincidentally controls SR Ca loading and SL Ca2+ efflux.
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影响因子：
4
作者：
Reuter, H;Henderson, SA;Philipson, KD
通讯作者：
Philipson, KD
影响因子：
5.5
作者：
TRAFFORD, AW;DIAZ, ME;EISNER, DA
通讯作者：
EISNER, DA
心脏钠钙交换的稳态和动态特性。细胞质钙和ATP的次要调节。
DOI：
10.1085/jgp.100.6.933
发表时间：
1992-12
期刊：
The Journal of general physiology
影响因子：
--
作者：
Hilgemann DW;Collins A;Matsuoka S
通讯作者：
Matsuoka S
影响因子：
3.4
作者：
Kappl, M;Hartung, K
通讯作者：
Hartung, K
影响因子：
10.8
作者：
NEGRETTI, N;ONEILL, SC;EISNER, DA
通讯作者：
EISNER, DA