Abstract：
:Hepatic fibrosis is caused by exaggerated wound healing response to chronic injury, which eventually leads to hepatic cirrhosis. Differentiation of hepatic stellate cells (HSCs) to myofibroblast-like cells by inflammatory cytokines is the critical step in fibrosis. This step is accompanied by enlargement of the endoplasmic reticulum (ER) and Golgi apparatus, suggesting that protein synthesis and secretion are augmented in the activated HSCs. However, the process of rearrangement of secretory organelles and their functions remain to be fully elucidated. Here, we revealed that differentiation alters early secretory gene expression. We observed significant isoform-specific upregulation of the inner coat protein complex II (COPII) components, Sec23A and Sec24D, via the transmembrane bZIP transcription factor, CREB3L2/BBF2H7, during HSC activation. Moreover, knockdown of these components abrogated the activation, suggesting that Sec23A/Sec24D-mediated ER to Golgi trafficking is required for HSC activation.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Tomoishi S,Fukushima S,Shinohara K,Katada T,Saito Kdoi
10.1038/s41598-017-08703-6subject
Has Abstractpub_date
2017-08-11 00:00:00pages
7992issue
1issn
2045-2322pii
10.1038/s41598-017-08703-6journal_volume
7pub_type
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