Abstract
Dynamics of a living body enables organs to experience mechanical stimulation at cellular level. Human cardiomyocytes cell line provides a source for simulating the heart dynamics; however, lack of understanding on mechanical stimulation effect on them limits potential applications. Here, we investigated the effect of mechanical stimulation on the cardiac function‐associated protein expressions in human cardiomyocytes. Human cardiomyocyte cell line AC16 was subjected to different stresses: 5% mild and 25% aggressive, at 1Hz for 24h. The stretched cardiomyocytes showed down‐regulated Piezo1, P‐AKTS473, and P‐GSK3bS9 compared to no stretch. In addition, the stretched cardiomyocytes showed increased LRP6, and P‐JNKT183/T185. When Piezo inhibitor was added to the cells during stretching, the LRP6, and P‐JNKT183/T185 were further increased under 25%, but not 5%, suggesting that higher mechanical stress further activated the Wnt‐related signaling pathway when Piezo1 was inhibited. Supporting this idea, we found expression of eNOS decreased, and release of calcium ions significantly reduced under 25% compared to 5%. These studies demonstrate that cyclic mechanical stimulation affects cardiac function‐associated protein expressions, and Piezo1 plays a role in the protein regulation.Support or Funding InformationThis research is supported by VGHKS107‐076, VGHKS107‐168, VGHKS107‐175, MOST104‐2320‐B‐0751B‐003‐MY3, and MOST106‐2320‐B‐075B‐001.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Highlights
The advancement for whole heart modelling is required for understanding cardiac dynamics; developing a whole heart model is difficult
To test the hypothesis that cardiomyocytes respond to mechanical stimulation, cells were subjected to 5% and 25% cyclic stretching at 1 Hz for 24 h
The Piezo1 protein expression decreased under both 5% and 25%
Summary
The advancement for whole heart modelling is required for understanding cardiac dynamics; developing a whole heart model is difficult. Mechanical stimulation has recently been applied to study cell dynamics in vitro. The goal of mechanical stimulation technology is to develop models that mimic in vivo dynamics. The hypertensive heart induces heart failure due to mechanical overloading greater than 140 mmHg [1]. Mechanical forces such as stretching, bending, and compression regulate cardiac structure and function [2]. The mechanically activated proteins may have roles in cardiac overloading; it has not been well studied in cardiac cells
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