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Independent roles of methionine sulfoxide reductase A in mitochondrial ATP synthesis and as antioxidant in retinal pigment epithelial cells. 蛋氨酸亚砜还原酶A在线粒体ATP合成和视网膜色素上皮细胞抗氧化剂中的独立作用。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-10-10 DOI: 10.1016/j.freeradbiomed.2013.10.006

Ying Dun, Jade Vargas, Nathan Brot, Silvia C Finnemann

{"title":"Independent roles of methionine sulfoxide reductase A in mitochondrial ATP synthesis and as antioxidant in retinal pigment epithelial cells.","authors":"Ying Dun, Jade Vargas, Nathan Brot, Silvia C Finnemann","doi":"10.1016/j.freeradbiomed.2013.10.006","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.10.006","url":null,"abstract":"The antioxidant enzyme methionine sulfoxide reductase A (MsrA) is highly expressed in the retinal pigment epithelium (RPE), a support tissue for neighboring photoreceptors. MsrA protein levels correlate with sensitivity of RPE in culture to experimental oxidative stress. To investigate whether and how MsrA affects RPE functionality regardless of oxidative stress, we tested the effects of acute silencing or overexpression of MsrA on the phagocytosis of photoreceptor outer segment fragments (POS), a demanding, daily function of the RPE that is essential for vision. Endogenous MsrA localized to mitochondria and cytosol of rat RPE in culture. RPE cells manipulated to express higher or lower levels of MsrA than control cells showed no signs of cell death but increased or decreased, respectively, POS binding as well as engulfment. These effects of altered MsrA protein concentration on phagocytosis were independent of the levels of oxidative stress. However, altering MsrA expression had no effect on phagocytosis when mitochondrial respiration was inhibited. Furthermore, ATP content directly correlated with MsrA protein levels in RPE cells that used mitochondrial oxidative phosphorylation for ATP synthesis but not in RPE cells that relied on glycolysis alone. Overexpressing MsrA was sufficient to increase specifically the activity of complex IV of the respiratory chain, whereas activity of complex II and mitochondrial content were unaffected. Thus, MsrA probably enhances ATP synthesis by increasing complex IV activity. Such contribution of MsrA to energy metabolism is independent of its function in protection from elevated oxidative stress but contributes to routine but vital photoreceptor support by RPE cells. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1340-1351"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.10.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31803533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Metabolic syndrome-induced tubulointerstitial injury: role of oxidative stress and preventive effects of acetaminophen. 代谢综合征诱导的小管间质损伤:氧化应激的作用和对乙酰氨基酚的预防作用。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-10-16 DOI: 10.1016/j.freeradbiomed.2013.10.005

Cuifen Wang, Eric R Blough, Ravikumar Arvapalli, Xiaoniu Dai, Satyanarayana Paturi, Nandini Manne, Hari Addagarla, William E Triest, Omolola Olajide, Miaozong Wu

{"title":"Metabolic syndrome-induced tubulointerstitial injury: role of oxidative stress and preventive effects of acetaminophen.","authors":"Cuifen Wang, Eric R Blough, Ravikumar Arvapalli, Xiaoniu Dai, Satyanarayana Paturi, Nandini Manne, Hari Addagarla, William E Triest, Omolola Olajide, Miaozong Wu","doi":"10.1016/j.freeradbiomed.2013.10.005","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.10.005","url":null,"abstract":"The prevalence of metabolic syndrome persistently increases and affects over 30% of U.S. adults. To study how metabolic syndrome may induce tubulointerstitial injury and whether acetaminophen has renal-protective properties, 4-week-old obese Zucker rats were randomly assigned into three groups, control (OC), vehicle dimethyl sulfoxide (OV), and acetaminophen treatment (30 mg/kg/day for 26 weeks), and lean Zucker rats served as healthy controls. Significant tubulointerstitial injuries were observed in both OC and OV animals, evidenced by increased tubular cell death, tubular atrophy/dilation, inflammatory cell infiltration, and fibrosis. These tubulointerstitial alterations were significantly reduced by treatment with a chronic but low dose of acetaminophen, which acted to diminish NADPH oxidase isoforms Nox2 and Nox4 and decrease tubulointerstitial oxidative stress (reduced tissue superoxide and macromolecular oxidation). Decreased oxidative stress by acetaminophen was paralleled by the reduction of tubular proapoptotic signaling (diminished Bax/Bcl-2 ratio and caspase 3 activation) and the alleviation of tubular epithelial-to-mesenchymal transition (decreased transforming growth factor β, connective tissue growth factor, α-smooth muscle actin, and laminin). These data suggest that increased oxidative stress plays a critical role in mediating metabolic syndrome-induced tubulointerstitial injury and provide the first evidence suggesting that acetaminophen may be of therapeutic benefit for the prevention of tubulointerstitial injury.","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1417-1426"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.10.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31820766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 26

Willow bark extract increases antioxidant enzymes and reduces oxidative stress through activation of Nrf2 in vascular endothelial cells and Caenorhabditis elegans. 柳树皮提取物通过激活血管内皮细胞和秀丽隐杆线虫的Nrf2，增加抗氧化酶，降低氧化应激。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2012-12-28 DOI: 10.1016/j.freeradbiomed.2012.12.006

Atsushi Ishikado, Yoko Sono, Motonobu Matsumoto, Stacey Robida-Stubbs, Aya Okuno, Masashi Goto, George L King, T Keith Blackwell, Taketoshi Makino

{"title":"Willow bark extract increases antioxidant enzymes and reduces oxidative stress through activation of Nrf2 in vascular endothelial cells and Caenorhabditis elegans.","authors":"Atsushi Ishikado, Yoko Sono, Motonobu Matsumoto, Stacey Robida-Stubbs, Aya Okuno, Masashi Goto, George L King, T Keith Blackwell, Taketoshi Makino","doi":"10.1016/j.freeradbiomed.2012.12.006","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2012.12.006","url":null,"abstract":"Willow bark extract (WBE) is listed in the European Pharmacopoeia and has been traditionally used for treating fever, pain, and inflammation. Recent studies have demonstrated its clinical usefulness. This study investigated the antioxidative effects of WBE in human umbilical vein endothelial cells (HUVECs) and Caenorhabditis elegans. WBE prevented oxidative-stress-induced cytotoxicity of HUVECs and death of C. elegans. WBE dose-dependently increased mRNA and protein expression levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) target genes heme oxygenase-1, γ-glutamylcysteine ligase modifier and catalytic subunits, and p62 and intracellular glutathione (GSH) in HUVECs. In the nematode C. elegans, WBE increased the expression of the gcs-1::green fluorescent protein reporter, a well-characterized target of the Nrf2 ortholog SKN-1, in a manner that was SKN-1-dependent. WBE increased intranuclear expression and DNA binding of Nrf2 and the activity of an antioxidant response element (ARE) reporter plasmid in HUVECs. WBE-induced expression of Nrf2-regulated genes and increased GSH levels in HUVECs were reduced by Nrf2 and p38 small interfering (si) RNAs and by the p38-specific inhibitor SB203580. Nrf2 siRNA reduced the cytoprotective effect of WBE against oxidative stress in HUVECs. Salicin, a major anti-inflammatory ingredient of WBE, failed to activate ARE-luciferase activity, whereas a salicin-free WBE fraction showed intensive activity. WBE induced antioxidant enzymes and prevented oxidative stress through activation of Nrf2 independent of salicin, providing a new potential explanation for the clinical usefulness of WBE. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1506-1515"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2012.12.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40201224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 62

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