Unknown

Dataset Information

0

CREB3L2-mediated expression of Sec23A/Sec24D is involved in hepatic stellate cell activation through ER-Golgi transport.

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.

SUBMITTER: Tomoishi S 

PROVIDER: S-EPMC5554210 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

CREB3L2-mediated expression of Sec23A/Sec24D is involved in hepatic stellate cell activation through ER-Golgi transport.

Tomoishi Shotaro S   Fukushima Shinichi S   Shinohara Kentaro K   Katada Toshiaki T   Saito Kota K  

Scientific reports 20170811 1

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 org  ...[more]

Similar Datasets

Unknown ULK1 phosphorylates Sec23A and mediates autophagy-induced inhibition of ER-to-Golgi traffic.
| S-EPMC5424413 | biostudies-literature
Unknown Biogenesis of tubular ER-to-Golgi transport intermediates.
| S-EPMC1356583 | biostudies-literature
Unknown Alpha-synuclein delays endoplasmic reticulum (ER)-to-Golgi transport in mammalian cells by antagonizing ER/Golgi SNAREs.
| S-EPMC2877643 | biostudies-literature
Unknown SEC23A confers ER stress resistance in gastric cancer by forming the ER stress-SEC23A-autophagy negative feedback loop.
| S-EPMC10478313 | biostudies-literature
Unknown A newly identified myomegalin isoform functions in Golgi microtubule organization and ER-Golgi transport.
| S-EPMC6518325 | biostudies-literature
Unknown Mitochondrial uncouplers inhibit hepatic stellate cell activation.
| S-EPMC3439697 | biostudies-literature
Unknown Epigenetic Changes during Hepatic Stellate Cell Activation.
| S-EPMC4466775 | biostudies-literature
Unknown Pharmacological Intervention in Hepatic Stellate Cell Activation and Hepatic Fibrosis.
| S-EPMC4764688 | biostudies-literature
Genomics Single-Cell Analysis Reveals Androgen Receptor Regulates ER-to-Golgi Trafficking with CREB3L2 To Drive Prostate Cancer Progression
2021-10-10 | GSE165562 | GEO
Unknown FFAT rescues VAPA-mediated inhibition of ER-to-Golgi transport and VAPB-mediated ER aggregation.
| S-EPMC3038994 | biostudies-literature