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Mechanical Stretching Simulates Cardiac Physiology and Pathology through Mechanosensor Piezo1
Author(s) -
Wong TzyyYue
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.374.9
Subject(s) - piezo1 , wnt signaling pathway , stimulation , protein kinase b , microbiology and biotechnology , pi3k/akt/mtor pathway , chemistry , enos , cell culture , signal transduction , endocrinology , medicine , biology , receptor , ion channel , biochemistry , mechanosensitive channels , nitric oxide synthase , enzyme , genetics
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‐AKT S473 , and P‐GSK3b S9 compared to no stretch. In addition, the stretched cardiomyocytes showed increased LRP6, and P‐JNK T183/T185 . When Piezo inhibitor was added to the cells during stretching, the LRP6, and P‐JNK T183/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 Information This 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 .