The dual role of osteopontin in acetaminophen hepatotoxicity

He, Chunyan; Liang, Beibei; Fan, Xiaoyu; Cao, Lei; Chen, Rui; Guo, Yajun; Zhao, Jian

doi:10.1038/aps.2012.47

Cited by 17 publications

(15 citation statements)

References 49 publications

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“…Moreover, OPN levels are associated with the degree of liver necrosis in acute liver injury; however, its involvement in preventing the progression of liver disease requires further investigation (Arai et al, 2006;Srungaram et al, 2015). In mice, OPN deficiency served to restrict neutrophil infiltration and macrophage accumulation and inhibited the release of pro-inflammatory cytokines (He et al, 2012). Similarly, by blocking OPN expression, the sensitivity to acetaminophen was reduced and mice developed the capacity to survive a drug overdose (Arai et al, 2006;He et al, 2012).…”

Section: Osteopontin (Opn)mentioning

confidence: 99%

“…In mice, OPN deficiency served to restrict neutrophil infiltration and macrophage accumulation and inhibited the release of pro-inflammatory cytokines (He et al, 2012). Similarly, by blocking OPN expression, the sensitivity to acetaminophen was reduced and mice developed the capacity to survive a drug overdose (Arai et al, 2006;He et al, 2012). However, another study evidenced that OPN improved the survival of hepatocytes in diethylnitrosamine-induced liver injury via inhibition of NF-kB activation and reduced production of inflammatory mediators .…”

Section: Osteopontin (Opn)mentioning

confidence: 99%

“…Basic studying data GLDH McGill et al, 2012;Harrill et al, 2012;Antoine et al, 2013;Schomaker et al, 2013;McGill et al, 2014;Singhal et al, 2014-K18 Koelink et al, 2009Possamai et al, 2013;Thulin et al, 2014;Xie et al, 2019Cummings et al, 2008SDH Harrill et al, 2012Metushi et al, 2012Metushi et al, 2014bGST Sun et al, 2008Singla et al, 2014;Cai et al, 2015;Wu et al, 2016a;Sun et al, 2017;Yang et al, 2019Giffen et al, 2002Bailey et al, 2012;Tsai et al, 2017BAs James et al, 2015Longo et al, 2019Yamazaki et al, 2013Qiu et al, 2016;Cepa et al, 2018CYP450 Sun et al, 2008Tang et al, 2013;Tang et al, 2013;Metushi et al, 2014a;Li et al, 2014Park et al, 2016OPN Arai et al, 2006Srungaram et al, 2015He et al, 2012Arriazu et al, 2017HMGB1 Antoine et al, 2012…”

Section: Biomarker Clinical Datamentioning

confidence: 99%

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Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Jiang

et al. 2020

Front. Pharmacol.

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Drug-induced liver injury (DILI) is one among the common adverse drug reactions and the leading causes of drug development attritions, black box warnings, and post-marketing withdrawals. Despite having relatively low clinical incidence, its potentially severe adverse events should be considered in the individual patients due to the high risk of acute liver failure. Although traditional liver parameters have been applied to the diagnosis of DILI, the lack of specific and sensitive biomarkers poses a major limitation, and thus accurate prediction of the subsequent clinical course remains a significant challenge. These drawbacks prompt the investigation and discovery of more effective biomarkers, which could lead to early detection of DILI, and improve its diagnosis and prognosis. Novel promising biomarkers include glutamate dehydrogenase, keratin 18, sorbitol dehydrogenase, glutathione S-transferase, bile acids, cytochrome P450, osteopontin, high mobility group box-1 protein, fatty acid binding protein 1, cadherin 5, miR-122, genetic testing, and omics technologies, among others. Furthermore, several clinical scoring systems have gradually emerged for the diagnosis of DILI including the Roussel Uclaf Causality Assessment Method (RUCAM), Clinical Diagnostic Scale (CDS), and Digestive Disease Week Japan (DDW-J) systems. However, currently their predictive value is limited with certain inherent deficiencies. Thus, perhaps the greatest benefit would be achieved by simultaneously combining the scoring systems and those biomarkers. Herein, we summarized the recent research progress on molecular biomarkers for DILI to improved approaches for its diagnosis and clinical management.

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Section: Osteopontin (Opn)mentioning

confidence: 99%

Section: Osteopontin (Opn)mentioning

confidence: 99%

Section: Biomarker Clinical Datamentioning

confidence: 99%

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Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Jiang

et al. 2020

Front. Pharmacol.

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“…Because APAP-induced hepatic injury occurs in several steps, KA and Ac 2 KA may exert protective effects against multiple steps of APAP action. Initially, we hypothesized that KA and Ac 2 KA were antioxidants, as the antioxidant natural products, which are known to prevent APAP-induced hepatic injury (6,8). Several investigations have reported that ent-kaurene diterpenoid compounds exert antioxidant activities (4,19).…”

Section: Discussionmentioning

confidence: 99%

1O, 20O-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in mice

et al. 2018

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The present study aimed to investigate the protective effects of kamebakaurin (KA) and 1O, 20O-diacetyl kamebakaurin (Ac 2 KA) on acetaminophen (APAP)-induced hepatotoxicity and compare the hepatoprotective mechanisms of the two chemicals. Seven-week-old male C57BL/6J mice were orally administered KA, Ac 2 KA, or an ethanol/olive oil emulsion once per day for 7-days. Twenty-four hours after the final administration, the mice were fasted and then intraperitoneally injected with 450 mg/kg APAP or saline. At 16 h after injection, the mice were euthanized and blood samples were collected for plasma analysis. Pretreatment with KA and Ac 2 KA significantly attenuated APAP-induced hepatic injury. The protective effect of Ac 2 KA was stronger than that of KA. These two chemicals attenuated oxidative stress, inflammatory cytokine production, c-jun N-terminal kinase activation, and receptor-interacting protein (RIP)-3 activation. Ac 2 KA also decreased APAP-induced RIP-1 activation and nuclear factor kappa B (NF-κB) p65 translocation. Moreover, Ac 2 KA repressed mRNA expression of Cyp1a2/2e1 in the liver. Our results showed that KA and Ac 2 KA exerted protective effects against APAP-induced hepatotoxicity. The responsible mechanisms may be related to the chemicals' antioxidant activity and the inhibition of c-jun N-terminal kinase activation and RIP-3 activation. The effects of Ac 2 KA included those of KA, as well as RIP-1 inactivation, NF-κB inhibition, and Cyp inhibition.

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“…213,214 Osteopontin has also proinflammatory effects by promoting the migration of macrophages and neutrophils. 200,215 In HCC osteopontin acts via different biological processes, contributing HCC metastasis, 216,217 proliferation, 218 EMT, 219,220 and resistance to apoptosis. 210,216…”

Section: Growth Factors and Cytokinesmentioning

confidence: 99%

Contributions of Fibroblasts, Extracellular Matrix, Stiffness, and Mechanosensing to Hepatocarcinogenesis

Filliol

Schwabe

2019

Semin Liver Dis

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Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide. A unique feature of liver cancer is its close association with liver fibrosis. About 90% of HCCs develop in advanced liver fibrosis or cirrhosis, suggesting an important role for the fibrotic microenvironment in driving HCC development. Here, the authors will discuss functional contributions of liver fibrosis to the development of HCC, focusing on mechanisms through which fibrosis may promote HCC development such as hepatic stellate cell-derived extracellular matrix, growth factors, and cytokines, stiffness-induced signaling pathways, and immunosuppression. Better understanding of these factors in HCC development and progression may provide the basis for novel stromal-based therapies for tumor prevention or therapy.

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The dual role of osteopontin in acetaminophen hepatotoxicity

Cited by 17 publications

References 49 publications

Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

<b>1</b><i><b>O</b></i><b>, 20</b><i><b>O</b></i><b>-diacetyl kamebakaurin protects against acetaminophen-induced hepatotoxicity in </b><b>mice </b>

Contributions of Fibroblasts, Extracellular Matrix, Stiffness, and Mechanosensing to Hepatocarcinogenesis

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