平滑筋のCa²⁺誘発収縮を調節する内在性心筋型トロポニンT

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.