Atrial-specific regulation of Ca2+ channel signalosome by a lipid-binding protein

脂质结合蛋白STARD 10在心房中表达并结合到L型Ca 2+通道，但在心室中不表达。 为了阐明心房中的Ca 2+通道信号体，我们分析了从野生型和STARD 10基因敲除小鼠中分离的体外心房及其肌细胞。 STARD 10的缺失增加了CaV1.2型L型Ca 2+电流的电流密度，增强了心房肌细胞的Ca 2+依赖性失活，但不改变α 1亚基CaV1.2的表达。 在野生型小鼠中，离体心房对机械拉伸的反应是收缩力的增加，而在基因敲除小鼠中，其自发放电率增加，收缩力的发展受到抑制。 结果提示，STARD 10可能调控心房肌L型Ca ~（2+）电流的Ca ~（2+）依赖性失活，其机制可能与机械牵张时心房肌收缩力的形成有关。

A lipid-binding protein, STARD10 is expressed and bound to L-type Ca2+ channel in the atrium but not in the ventricle. To clarify the Ca2+ channel signalosome in the atria, we analyzed the atria and their myocytes in vitro which are isolated from wild-type and STARD10 knock-out mice. The loss of STARD10 increased the current density of CaV1.2-type L-type Ca2+ currents with the enhancement of Ca2+-dependent inactivation in the atrial myocytes, but it did not change the expression of alpha1 subunit CaV1.2. The response of the isolated atria to a mechanical stretch was an increase in the contraction force in wild-type mice, while it was an increase in the rate of its spontaneous firing with suppression of development in the contraction force in knock-out mice. The results suggested that STARD10 may regulate Ca2+-dependent inactivation of atrial L-type Ca2+ current, and that the mechanism may contribute the atrial contraction force development in response to mechanical stretch.