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Pubmed ID :28970837
Publication Date : //

Lysosomal Ca Signaling Regulates High Glucose-Mediated Interleukin-1β Secretion Transcription Factor EB in Human Monocytic Cells.


Aberrant activation of the innate immune system, including NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome-dependent interleukin-1β (IL-1β) secretion, has been implicated in the pathogenesis of type 2 diabetes mellitus (T2DM) and its complication. Our previous study demonstrated that hyperglycemia, a hallmark characteristic of T2DM, induced NLRP3 inflammasome-dependent caspase-1 activation and IL-1β maturation in human monocytic cells. In this study, we examined the underlying mechanisms of secreting IL-1β during hyperglycemia, with a focus on the alteration of Ca homeostasis and lysosomal exocytosis. We found that high glucose (HG; 30 mM glucose for 48 h) altered Ca homeostasis by reducing lysosomal Ca concentration that appeared to be resulted from Ca moving out of lysosomes into cytosol in human monocytic cell lines, U937 and THP-1 cells. Moreover, HG-induced lysosomal Ca-dependent mature IL-1β release was strongly correlated with the activation and upregulation of two lysosomal marker proteins, cathepsin D and lysosomal-associated membrane protein-1 (LAMP-1). This involved calcineurin/transcription factor EB (TFEB) pathway and its target genes, cathepsin B, cathepsin D, and LAMP-1, to mediate lysosomal exocytosis. Therefore in this study, we revealed a novel mechanism of HG-induced lysosomal exocytosis which was regulated by lysosomal Ca signals through calcineurin/TFEB pathway, thus contributing to IL-1β secretion in human monocytic cells.

Authors : Tseng Hisa Hui Ling , Vong Chi Teng , Kwan Yiu Wa , Lee Simon Ming-Yuen , Hoi Maggie Pui Man ,

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