The role of Hepassocin in the development of non-alcoholic fatty liver disease

Wu, Hung Tsung; Lu, Feng Hwa; Ou, Horng Yih; Su, Yu; Hung, Hao Chang; Wu, Jin Shang; Yang, Yi Ching; Wu, Chao; Chang, Chih Jen

doi:10.1016/j.jhep.2013.06.004

Cited by 75 publications

(92 citation statements)

References 26 publications

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“…FGL1 is a hepatocyte secreted protein containing a fibrinogen-related domain in its C-terminal portion [19]. The enhancement of FGL1 levels was regulated by IL-6 [20, 21] and it participates in the development of non-alcoholic fatty liver disease, hepatocellular carcinomas, and hepatocyte mitogenic activity [22–26]. However, there are no reports of the involvement of any of these genes in EMT or fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Identification of molecular signatures involved in radiation-induced lung fibrosis

et al. 2018

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In radiotherapy, radiation (IR)-induced lung fibrosis has severe and dose-limiting side effects. To elucidate the molecular effects of IR fibrosis, we examined the fibrosis process in irradiated mouse lung tissues. High focal IR (90 Gy) was exposed to a 3-mm volume of the left lung in C57BL6 mice. In the diffused irradiation, 20 Gy dose delivered with a 7-mm collimator almost covered the entire left lung. Histological examination for lung tissues of both irradiated and neighboring regions was done for 4 weeks after irradiation. Long-term effects (12 months) of 20Gy IR were compared on a diffuse region of the left lung and non-irradiated right lung. Fibrosis was initiated as early as 2 weeks after IR in the irradiated lung region and neighboring region. Upregulation of gtse1 in both 90Gy-irradiated and neighboring regions was observed. Upregulation of fgl1 in both 20Gy diffused irradiated and non-irradiated lungs was identified. When gtse1 or flg1 was knock-downed, TGFβ or IR-induced epithelial-mesenchymal transition was inhibited, accompanied with the inhibition of cellular migration, suggesting fibrosis responsible genes. Immunofluorescence analysis using mouse fibrotic lung tissues suggested that fibrotic regions showed increased expressions of Gtse1 and Fgl1, indicating novel molecular signatures of gtse1and fgl1 for IR-induced lung fibrosis. Even though their molecular mechanisms and IR doses or irradiated volumes for lung fibrosis may be different, these genes may be novel targets for understanding IR-induced lung fibrosis and in treatment strategies.Key messages Upregulation of gtse1 by 90Gy focal irradiation and upregulation of fgl1 by 20Gy diffused irradiation are identified in mouse lung fibrosis model.Gtse1 and Fgl1 are involved in radiation or TGFβ-induced epithelial-mesenchymal transition.Radiation-induced fibrotic regions of mouse lungs showed increased expressions of Gtse1 and Fgl1.Gtse1 and Fgl1 are suggested to be novel targets for radiation-induced lung fibrosis. Electronic supplementary materialThe online version of this article (10.1007/s00109-018-1715-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Identification of molecular signatures involved in radiation-induced lung fibrosis

et al. 2018

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“…Recently, a study suggested a previously unrecognized role for HPS in regulation of intermediate metabolism [8,9]. HPS knockout mice showed an overall glucose and lipid metabolism disorder not observed in wild type mice.…”

Section: Resultsmentioning

confidence: 99%

“…Recent studies have shown that gene ablation of HPS in mice results in abnormal plasma lipid profiles, fasting hyperglycemia with enhanced gluconeogenesis, and differences in white and brown adipose tissue morphology [8], indicating that HPS is a member of an emerging group of proteins that have key roles in metabolism. Studies have provided evidence Abbreviations: GATA6, GATA-binding factor 6; Hhex, hematopoieticallyexpressed homeobox protein; FGL1, Fibrinogen-like 1; IL-6, interleukin-6; HNF1a, hepatocyte nuclear factor1a; HCC, Hepatocellular Carcinoma; Fabp10, fatty acidbinding protein 10. that HPS plays an important role in non-alcoholic fatty liver disease (NAFLD) and induces hepatic lipid accumulation through an ERK1/ 2-dependent pathway [9].…”

Section: Introductionmentioning

confidence: 99%

“…Liver development in zebrafish is similar to that in mammals and other vertebrates but they do not generally experience hematopoietic defects [10e12]. In mammals, HPS signaling was found to promote hepatocyte proliferation, protect hepatocytes from injury, and regulate lipid metabolism [2,8,9]. However, the function of HPS in zebrafish livers is not yet well understood.…”

Section: Introductionmentioning

confidence: 99%

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Hepassocin is required for hepatic outgrowth during zebrafish hepatogenesis

Gao

Yan²,

Yin

et al. 2015

Biochemical and Biophysical Research Communications

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“…Hepassocin (HPS), a hepatokine, is elevated in serum of NAFLD patients. High expressing HPS induces NAFLD in transgenic mice, and facilitates lipid accumulation in HepG2 cells, in an ERK1/2-dependent manner [33]. It has been reported that liver specific deletion of PTEN expression activates Akt and enhances the development of fatty liver [34].…”

Section: Discussionmentioning

confidence: 99%

Activation of hepatic Nogo-B receptor expression—A new anti-liver steatosis mechanism of statins

Zhang

Yang

Chen

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Deficiency of hepatic Nogo-B receptor (NgBR) expression activates liver X receptor α (LXRα) in an adenosine monophosphate-activated protein kinase α (AMPKα)-dependent manner, thereby inducing severe hepatic lipid accumulation and hypertriglyceridemia. Statins have been demonstrated non-cholesterol lowering effects including anti-nonalcoholic fatty liver disease (NAFLD). Herein, we investigated if the anti-NAFLD function of statins depends on activation of NgBR expression. In vivo, atorvastatin protected apoE deficient or NgBR floxed, but not hepatic NgBR deficient mice, against Western diet (WD)-increased triglyceride levels in liver and serum. In vitro, statins reduced lipid accumulation in nonsilencing small hairpin RNA-transfected Conflict of interestNone declared. Transparency documentThe http://dx.doi.org/10.1016/j.bbalip.2017.12.002 associated with this article can be found, in online version. HHS Public Access

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The role of Hepassocin in the development of non-alcoholic fatty liver disease

Cited by 75 publications

References 26 publications

Identification of molecular signatures involved in radiation-induced lung fibrosis

Identification of molecular signatures involved in radiation-induced lung fibrosis

Hepassocin is required for hepatic outgrowth during zebrafish hepatogenesis

Activation of hepatic Nogo-B receptor expression—A new anti-liver steatosis mechanism of statins

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