This study demonstrates, using an in vitro motility assay, that a brief, focused infrared‑laser pulse (λ = 1,455 nm) can activate cardiac thin filaments independently of Ca²⁺. Thin filaments reconstituted with human α‑tropomyosin and bovine ventricular troponin were observed gliding on rabbit fast‑skeletal myosin HMM. When temperature was shifted from 25 °C to ≈ 46 °C within 0.2 s, filament sliding occurred even in the absence of Ca²⁺, and velocity increased proportionally with temperature.
With Ca²⁺ present, sliding velocity also rose, but its temperature dependence was roughly halved. This suggests that near body temperature (~ 37 °C) the thin‑filament on–off equilibrium is already partially shifted toward the “on” state, enabling rapid, energy‑efficient contraction with only minimal Ca²⁺ elevation.
Local temperature was measured precisely by combining fluorescence of rhodamine–phalloidin–labeled actin with a EuTTA‑based fluorescent thermometer sheet. Reversible filament motion was confirmed after heating and cooling without protein denaturation. The temperature coefficient Q₁₀ was high (5.5) without Ca²⁺ and dropped to 1.9 with Ca²⁺ present, implicating the troponin–tropomyosin complex as the key temperature sensor.
These findings offer molecular insight into how fever or targeted heating affects cardiac function and may inspire temperature‑based therapeutic strategies for heart failure.
Article information & citation
Shuya Ishii, Kotaro Oyama, Tomomi Arai, Hideki Itoh, Seine A Shintani, Madoka Suzuki, Fuyu Kobirumaki-Shimozawa, Takako Terui, Norio Fukuda, Shin'ichi Ishiwata. Microscopic heat pulses activate cardiac thin filaments. Journal of general physiology, 151(6), 860-869, 2019.