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    Area of Science:

    • Cardiovascular Biology
    • Cellular Mechanotransduction
    • Molecular Cardiology

    Background:

    • Pathologic cardiac hypertrophy necessitates increased protein synthesis, but the mechanosensors linking membrane stretch to translation remain unclear.
    • Polycystin-1 (PC1) is a candidate cardiac mechanosensor, with its C-terminal tail (PC1-CT) implicated in cardiomyocyte hypertrophy, though its precise role and signaling are poorly defined in human cells.

    Purpose of the Study:

    • To investigate the subcellular localization of endogenous PC1 C-terminus and the downstream signaling effects of PC1-CT overexpression in human and mouse cardiomyocytes.
    • To elucidate the molecular mechanisms by which PC1-CT influences cardiomyocyte growth and protein synthesis.

    Main Methods:

    • Immunofluorescence microscopy to determine PC1-CT localization in human iPSC-derived ventricular cardiomyocytes (hiPSC-CMs) and adult mouse ventricular myocytes.
    • RNA sequencing (RNA-seq) and Gene Set Enrichment Analysis (GSEA) to analyze transcriptional changes following PC1-CT overexpression in hiPSC-CMs.
    • Pharmacological inhibition of PI3K and MEK pathways to dissect the signaling cascade downstream of PC1-CT.

    Main Results:

    • PC1-CT exhibits a striated pattern, localizing between α-actinin bands in hiPSC-CMs and colocalizing with sarcomeric proteins in adult myocytes, indicating maturation-dependent distribution.
    • PC1-CT overexpression upregulated gene sets for ribosome biogenesis and protein synthesis, but not canonical hypertrophic markers.
    • PC1-CT activated the PI3K-Akt-mTOR-S6K1-S6 signaling pathway, evidenced by increased phosphorylation of Akt, S6K1, and S6, independent of G i/o signaling.

    Conclusions:

    • A sarcomere-associated pool of PC1-CT engages PI3K-Akt-mTOR-S6K1-S6 signaling to promote ribosome biogenesis and protein synthesis.
    • PC1-CT enhances cardiomyocyte growth through specific signaling pathways without activating a classical hypertrophic gene program.
    • These findings establish a mechanistic link between PC1-CT and cardiomyocyte growth regulation.