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• W2556444382 abstract "The histidine-rich calcium-binding protein (HRC) is a regulator of Ca2+ homeostasis and it plays a significant role in hepatocellular carcinoma (HCC) progression. However, the relationship between HRC and liver fibrogenesis is still unknown. Our data demonstrates that HRC was upregulated in fibrotic liver and activated hepatic stellate cells (HSCs). TGF-β treatment increased α-SMA and HRC expression dose-dependently in HSCs. Repression of HRC reduced α-SMA, CTGF and collagen expression, and inhibited HSC proliferation and migration. In addition, we found that the anti-fibrosis effect of HRC knockdown was associated with endoplasmic reticulum (ER) stress. Silencing of HRC decreased the expression of ER stress and autophagy markers. Moreover, ER stress agonist thapsigargin (TG) enhanced, whereas ER stress antagonist 4-phenylbutyric acid (4-PBA) alleviated HSCs activation and autophagy. In conclusion, these data indicate that depletion of HRC inhibited HSC activation through the ER stress pathway, and HRC may be a potential regulator of liver fibrosis." @default.
• W2556444382 created "2016-11-30" @default.
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• W2556444382 date "2016-01-01" @default.
• W2556444382 modified "2023-10-16" @default.
• W2556444382 title "Knockdown of histidine-rich calcium binding protein (HRC) suppresses liver fibrosis by inhibiting the activation of hepatic stellate cells" @default.
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• W2556444382 doi "https://doi.org/10.1242/bio.019828" @default.
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