Endogenous cardiac troponin T modulates Ca(2+)-mediated smooth muscle contraction.

Endogenous cardiac troponin T modulates Ca(2+)-mediated smooth muscle contraction.
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DOI:
10.1038/srep00979
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发表时间:
2012
期刊:
影响因子:
4.6
通讯作者:
Naito, Seiji
Naito, Seiji
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Kajioka, Shunichi;Takahashi-Yanaga, Fumi;Shahab, Nouval;Onimaru, Mitsuho;Matsuda, Miho;Takahashi, Ryosuke;Asano, Haruhiko;Morita, Hiromitsu;Morimoto, Sachio;Yonemitsu, Yoshikazu;Hayashi, Maya;Seki, Narihito;Sasaguri, Toshiuyki;Hirata, Masato;Nakayama, Shinsuke;Naito, Seiji

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长期以来,人们一直认为与肌动蛋白丝相关的机制与平滑肌收缩有关,尽管关键分子尚不清楚。我们显示的证据表明,心脏肌钙蛋白T (cTnT)在细胞质Ca2+浓度的生理范围内实质性地促进Ca2+介导的收缩([Ca2+]i)。在包括人类在内的主动脉、气管、肠道和膀胱的各种平滑肌中检测到cTnT。此外,cTnT与原肌球蛋白一起分布在平滑肌细胞中,表明这些蛋白已准备好引起平滑肌收缩。在cTnT+/ -小鼠的化学渗透性平滑肌中,cTnT减少到~50%,Ca2+-力关系向更大的[Ca2+]i转移,表明cTnT对[Ca2+]i < 1 μM的平滑肌收缩有相当大的贡献。此外,补充TnI和TnC重建肌钙蛋白系统,以增强收缩。结果表明,肌动蛋白丝上的Tn/Tn样系统与粗丝途径协同作用。
Mechanisms linked to actin filaments have long been thought to cooperate in smooth muscle contraction, although key molecules were unclear. We show evidence that cardiac troponin T (cTnT) substantially contributes to Ca2+-mediated contraction in a physiological range of cytosolic Ca2+ concentration ([Ca2+]i). cTnT was detected in various smooth muscles of the aorta, trachea, gut and urinary bladder, including in humans. Also, cTnT was distributed along with tropomyosin in smooth muscle cells, suggesting that these proteins are ready to cause smooth muscle contraction. In chemically permeabilised smooth muscle of cTnT+/− mice in which cTnT reduced to ~50%, the Ca2+-force relationship was shifted toward greater [Ca2+]i, indicating a sizeable contribution of cTnT to smooth muscle contraction at [Ca2+]i < 1 μM. Furthermore, addition of supplemental TnI and TnC reconstructed a troponin system to enhance contraction. The results indicated that a Tn/Tn-like system on actin-filaments cooperates together with the thick-filament pathway.
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