Identification of a novel biomarker for oxidative stress induced by hydrogen peroxide in primary human hepatocytes using the 2‐nitrobenzenesulfenyl chloride isotope labeling method

Takami, Yoichiro; Uto, Hirofumi; Tamai, Tsutomu; Satô, Yukô; Ishida, Yoichi; Morinaga, Hiroyuki; Sakakibara, Yoichi; Moriuchi, Akihiro; Oketani, Makoto; Ido, Akio; Nakajima, Tomoaki; Okanoue, Takeshi; Tsubouchi, Hirohito

doi:10.1111/j.1872-034x.2009.00615.x

Cited by 18 publications

(10 citation statements)

References 31 publications

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“…Previous experiments showed that the expression of MnSOD was decreased when retinal ganglion cells were treated with hydrogen peroxide ( Khan et al, 2012 ). However, in primary hepatocytes and human macrophages, the expression of MnSOD was increased when the cells were treated with hydrogen peroxide ( Kinscherf et al, 1998 ; Takami et al, 2010 ). Also, no significant change of MnSOD was observed when pancreatic beta cells were treated with hydrogen peroxide ( Kimoto et al, 2003 ).…”

Section: Discussionmentioning

confidence: 99%

miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase

Long

Gan

Zhang

et al. 2017

Molecules and Cells

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Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.

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Section: Discussionmentioning

confidence: 99%

miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase

Long

Gan

Zhang

et al. 2017

Molecules and Cells

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“…Serum concentrations of cytokeratin 18 fragment [94], adiponectin [95], high sensitivity CRP [96], thioredoxin [97], and MnSOD [98] are useful for diagnosis of NASH. In a large-scale study, cytokeratin 18 fragment was shown to a useful single diagnostic marker for NASH [99].…”

Section: Blood Biomarkersmentioning

confidence: 99%

Clinical features of hepatocellular carcinoma associated with nonalcoholic fatty liver disease: a review of human studies

Oda

Uto

Mawatari

et al. 2015

Clin J Gastroenterol

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Most cases of hepatocellular carcinoma (HCC) in Japan develop in the background of chronic liver disease caused by hepatitis C virus (HCV). Recently, however, HCV-associated HCC has been shown to be decreasing, while non-B and non-C HCC (NBNC-HCC), which is negative for HCV and hepatitis B virus infection, has increased. The main cause of NBNC-HCC is alcoholic liver disease, but the recent increase of NBNC-HCC is thought to be due to an increase in patients with nonalcoholic fatty liver disease (NAFLD). Approximately 10% of NAFLD cases involve nonalcoholic steatohepatitis (NASH), and NASH can progress to liver cirrhosis and its associated complications such as HCC. There are no accurate data on the percentage of NASH-related HCC among all-cause HCC in Japan, because no large-scale investigation has been performed. However, the rate is thought to be about 3% of overall HCC, which is lower than that in the United States. The incidence of HCC in patients with NASH-related cirrhosis is thought to be 2% per year, which is lower than that in HCV-related cirrhosis. Risks for NASH-related HCC include advanced hepatic fibrosis, older age, and being male. NAFLD that includes NASH is associated with metabolic syndrome, which includes obesity and diabetes, and metabolic syndrome is a risk factor for HCC. Genetic factors and dietary patterns may also be related to NASH-related HCC. Thus, regular HCC surveillance, as performed for patients with viral chronic liver disease, is required for patients with NAFLD, and diagnostic markers are required for simple, rapid and specific detection of NASH-related HCC.

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“…Takami Y. et al . (2010) showed that systemic MnSOD protein is significantly higher in NASH patients than in steatotic patients and healthy controls [ 98 ]. A case–control and intra-familial allele association studies prove the evidence that carriage of the rs4880 polymorphism involved in determining the susceptibility to oxidative stress and fibrogenesis, respectively, have been associated with the severity of liver fibrosis in adults and children with NAFLD [ 99 ].…”

Section: Manganese Superoxide Dismutase Gene ( Mnsod mentioning

confidence: 99%

Gene polymorphisms associated with non-alcoholic fatty liver disease and coronary artery disease: a concise review

Sui

et al. 2016

Lipids Health Dis

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Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease which represents a wide spectrum of hepatic damage. Several studies have reported that NAFLD is a strong independent risk factor for coronary artery disease (CAD). And patients with NAFLD are at higher risk and suggested undergoperiodic cardiovascular risk assessment. Cardiovascular disease (CVD) is responsible for the main cause of death in patients with NAFLD, and is mostly influenced by genetic factors. Both NAFLD and CAD are heterogeneous disease. Common pathways involved in the pathogenesis of NAFLD and CAD includes insulin resistance (IR), atherogenic dyslipidemia, subclinical inflammation, oxidative stress, etc. Genomic characteristics of these two diseases have been widely studied, further research about the association of these two diseases draws attention. The gene polymorphisms of adiponectin-encoding gene (ADIPOQ), leptin receptor (LEPR), apolipoprotein C3 (APOC3), peroxisome proliferator-activated receptors (PPAR), sterol regulatory elementbinding proteins (SREBP), transmembrane 6 superfamily member 2 (TM6SF2), microsomal triglyceride transfer protein (MTTP), tumor necrosis factors-alpha (TNF-α) and manganese superoxide dismutase (MnSOD) have been reported to be related to NAFLD and CAD. In this review, we aimed to provide an overview of recent insights into the genetic basis of NAFLD and CAD.

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Identification of a novel biomarker for oxidative stress induced by hydrogen peroxide in primary human hepatocytes using the 2‐nitrobenzenesulfenyl chloride isotope labeling method

Abstract: The NBS labeling technique was useful to identify biomarkers. Serum MnSOD may be a useful biomarker that can distinguish between SS and NASH.

Cited by 18 publications

References 31 publications

miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase

miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase

Clinical features of hepatocellular carcinoma associated with nonalcoholic fatty liver disease: a review of human studies

Gene polymorphisms associated with non-alcoholic fatty liver disease and coronary artery disease: a concise review

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