Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 8, Pages -Publisher
MDPI
DOI: 10.3390/ijms23084146
Keywords
TRPV4 ion channel; exocytosis; A375 cell; Ca2+ signaling; ferroptosis
Funding
- National Natural Science of Foundation in China [81301720]
- Scientific Research Fund of Educational Department of Liaoning Province [LZ2020019]
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Activation of TRPV4 leads to massive exocytosis in melanoma cells, which is mediated by the entry of calcium ions through TRPV4. The interaction between TRPV4 and folding/vesicle trafficking proteins enhances exocytosis.
TRPV4 (transient receptor potential vanilloid 4), a calcium permeable TRP ion channel, is known to play a key role in endocytosis. However, whether it contributes to exocytosis remains unclear. Here, we report that activation of TRPV4 induced massive exocytosis in both melanoma A375 cell and heterologous expression systems. We show here that, upon application of TRPV4-specific agonists, prominent vesicle priming from endoplasmic reticulum (ER) was observed, followed by morphological changes of mitochondrial crista may lead to cell ferroptosis. We further identified interactions between TRPV4 and folding/vesicle trafficking proteins, which were triggered by calcium entry through activated TRPV4. This interplay, in turn, enhanced TRPV4-mediated activation of folding and vesicle trafficking proteins to promote exocytosis. Our study revealed a signaling mechanism underlying stimulus-triggered exocytosis in melanoma and highlighted the role of cellular sensor TRPV4 ion channel in mediating ferroptosis.
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