Molecular and biophysical mechanisms of Ca2+ sparklets in smooth muscle.
Molecular and biophysical mechanisms of Ca2+ sparklets in smooth muscle.
复制标题
平滑肌中 Ca2 火花的分子和生物物理机制。
DOI：
10.1016/j.yjmcc.2009.07.008
复制
发表时间：
2009
影响因子：
5
通讯作者：
Navedo,ManuelF
中科院分区：
文献类型：
--
作者：
Santana,LuisF;Navedo,ManuelF
In this article, we review the biophysical basis and functional implications of a novel Ca2+signal (called “Ca2+sparklets”) produced by Ca2+influx via L-type Ca2+channels (LTCCs) in smooth muscle. Ca2+sparklet activity is bimodal. In low activity mode, Ca2+sparklets are produced by random, brief openings of solitary LTCCs. In contrast, small clusters of LTCCs can function in a high activity mode that creates sites of continual Ca2+influx called “persistent Ca2+sparklets”. Low activity and persistent Ca2+sparklets contribute to Ca2+influx in arterial, colonic, and venous smooth muscle. Targeting of PKCα by the scaffolding protein AKAP150 to specific sarcolemmal domains is required for the activation of persistent Ca2+sparklets. Calcineurin, which is also associated with AKAP150, opposes the actions of PKCα on Ca2+sparklets. At hyperpolarized potentials, Ca2+sparklet activity is low and hence does not contribute to global [Ca2+]i. Membrane depolarization increases low and persistent Ca2+sparklet activity, thereby increasing local and global [Ca2+]i. Ca2+sparklet activity is increased in arterial myocytes during hypertension, thus increasing Ca2+influx and activating the transcription factor NFATc3. We discuss a model for subcellular variations in Ca2+sparklet activity and their role in the regulation of excitation–contraction coupling and excitation–transcription coupling in smooth muscle.
