Key result
Cardiac troponin T deficiency significantly reduced Ca2+-mediated force development in permeabilized smooth muscle at 0.5 μM [Ca2+]i from 2.84 mg to 1.94 mg (P=0.0017).
Absolute Event Rate: 1.94% vs 2.84%
p-value: p=0.0017
Cardiac troponin T is expressed in smooth muscle and substantially contributes to Ca2+-mediated contraction at physiological intracellular calcium concentrations.
Should not change clinical practice; leaves open cardiac troponin T's role in human smooth muscle contractility.
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 Ca(2+)-mediated contraction in a physiological range of cytosolic Ca(2+) concentration ([Ca(2+)](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 Ca(2+)-force relationship was shifted toward greater [Ca(2+)](i), indicating a sizeable contribution of cTnT to smooth muscle contraction at [Ca(2+)](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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Kajioka et al. (2012) studied Normal voiding function (patients undergoing cystectomy for bladder cancer) (n=12). cTnT deficiency (cTnT+/- mice) vs. Wild-type (cTnT+/+) mice was evaluated on Force development at 0.5 μM [Ca2+]i in chemically permeabilized detrusor strips (p=0.0017). Cardiac troponin T deficiency significantly reduced Ca2+-mediated force development in permeabilized smooth muscle at 0.5 μM [Ca2+]i from 2.84 mg to 1.94 mg (P=0.0017).
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