Turkish Journal of Zoology




We investigated the effect of endoplasmic reticulum (ER) protein 29 (ERp29) on thyroglobulin (Tg) secretion and its negative regulation by microRNAs (miRNAs). ERp29 overexpression promoted Tg secretion from thyrocytes of PCCL3 cells via activation of ER stress sensors, including activation of transcription factor 6 fragmentation, XBP1 mRNA splicing by inositol-requiring enzyme 1, and phosphorylation of eukaryotic initiation factor 2 alpha as downstream actions of RNA-dependent protein kinase-like ER kinase. Thyroid hormone receptor beta is a target gene of mir-331, one of the most abundant miRNAs observed in ERp29-overexpressing cells. mir-331 negatively regulated Tg expression and secretion by ~70% compared with the control. To overcome hypothyroidism, Tg secretion at the molecular level is required to counteract negative regulation of intracellular mir-331. Our findings may provide insight into the treatment of diseases caused by poor ER protein secretion, including ER storage disease.


PCCL3 cells, endoplasmic reticulum stress, ERp29, thyroglobulin, mir-331

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