Vitamin D3 up-regulated protein 1 （VDUP1） is a multifunctional protein involved in maintaining cellular homeostasis. VDUP1 is induced by a variety of stresses. Inversely, VDUP1 is often reduced in various tumor tiss...Vitamin D3 up-regulated protein 1 （VDUP1） is a multifunctional protein involved in maintaining cellular homeostasis. VDUP1 is induced by a variety of stresses. Inversely, VDUP1 is often reduced in various tumor tissues and cell lines. Over-expression of VDUP1 inhibits cell proliferation through cell cycle arrest. VDUP1 interacts with thioredoxin （Trx） and negatively regulates the expression and antioxidant function of Trx which is involved in redox regulation. VDUP1/ mice are more susceptible to carcinogenesis than wild-type mice and are defective in establishing immune system induding the development and function of natural killer cells. Furthermore, VDUP1^-/- mice show impaired Kreb cycle-mediated fatty acid utilization. In this review, we have discussed the multifunctional roles of VDUP1 in diverse cellular responses, in particular its relation to proliferation, apoptosis, differentiation, and diseases such as cancer and stress-related diseases.展开更多
Reactive oxygen species (ROS) are produced under oxidative stress, such as high oxygen concentration and during the metabolic consumption of oxygen molecules. Male reproductive tissues appear to be continuously expose...Reactive oxygen species (ROS) are produced under oxidative stress, such as high oxygen concentration and during the metabolic consumption of oxygen molecules. Male reproductive tissues appear to be continuously exposed to ROS produced by active metabolism. In addition, spermatozoa must pass through a high oxygen environment during the mating process. Thus, to maintain viable reproductive ability, a protective mechanism against oxidative stress is of importance. Here, we overview our current understanding of the cooperative function of antioxidative and redox systems that are involved in male fertility. Superoxide dismutase and glutathione peroxidase are major enzymes that scavenge harmful ROS in male reproductive organs. In turn, glutathione and thioredoxin systems constitute the main redox systems that repair oxidized and damaged molecules and also play a role in regulating a variety of cellular functions. While glutathione functions as an antioxidant by donating electrons to glutathione peroxidase and thioredoxin donates electrons to peroxiredoxin as a counterpart of glutathione peroxidase. In addition, aldo-keto reductases, which detoxify carbonyl compounds produced by oxidative stress, are present at high levels in the epithelia of the genital tract and Sertoli cells of the testis. Since these systems are involved in cross-talk, a comprehensive understanding will be required to maintain the physiological functions of male reproductive system.展开更多
Sugarcane mosaic virus （SCMV） causes substantial losses of grain yield and forage biomass in susceptible maize worldwide. A major quantitative trait locus, Scmvl, has been identified to impart strong resistance to S...Sugarcane mosaic virus （SCMV） causes substantial losses of grain yield and forage biomass in susceptible maize worldwide. A major quantitative trait locus, Scmvl, has been identified to impart strong resistance to SCMV at the early infection stage. Here, we demonstrate that ZmTrxh, encoding an atypical h-type thioredoxin, is the causal gene at Scmvl, and that its transcript abundance correlated strongly with maize resistance to SCMV. ZmTrxh alleles, whether they are resistant or susceptible, share the identical coding/proximal promoter regions, but vary in the upstream regulatory regions. ZmTrxh lacks two canon- ical cysteines in the thioredoxin active-site motif and exists uniquely in the maize genome. Because of this, ZmTrxh is unable to reduce disulfide bridges but possesses a strong molecular chaperone-like activity. ZmTrxh is dispersed in maize cytoplasm to suppress SCMV viral RNA accumulation. Moreover, ZmTrxh- mediated maize resistance to SCMV showed no obvious correlation with the salicylic acid- and jasmonic acid-related defense signaling pathways. Taken together, our results indicate that ZmTrxh exhibits a distinct defense profile in maize resistance to SCMV, differing from previously characterized dominant or recessive potyvirus resistance genes.展开更多
Background Obstructive sleep apnea （OSA） can cause cognitive dysfunction and may be a reversible cause of cognitive loss in patients with Alzheimer＇s disease （AD）. Chronic exposure to intermittent hypoxia （IH）,...Background Obstructive sleep apnea （OSA） can cause cognitive dysfunction and may be a reversible cause of cognitive loss in patients with Alzheimer＇s disease （AD）. Chronic exposure to intermittent hypoxia （IH）, such as encountered in OSA, is marked by neurodegenerative changes in rat brain. We investigated the change of thioredoxin （Trx）, spatial learning and memory in rats exposed to chronic intermittent hypoxia （CIH）. Methods Forty healthy male Sprague-Dawley （SD） rats were randomly divided into four groups of ten each： a CIH＋normal saline （CIH＋NS group）, a N-acetylcystein-treated CIH （CIH＋NAC） group, a sham CIH group （sham CIH＋NS）, and a sham NAC-treated sham CIH （CIH＋NAC） group. Spatial learning and memory in each group was assessed with the Morris water maze. Real-time PCR and Western blotting were used to examine mRNA and protein expression of Trx in the hippocampus tissue. The terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling （TUNEL） method was used to detect the apoptotic cells of the hippocampus CA1 region. Results CIH-rats showed impaired spatial learning and memory in the Morris water maze, including longer mean latencies for the target platform, reduced numbers of passes over the previous target platform and a smaller percentage of time spent in the target quadrant. Trx mRNA and protein levels were significantly decreased in the CIH-hippocampus, meanwhile, an elevated apoptotic index revealed apoptosis of hippocampal neurons of rats exposed to CIH. The rats, which acted better in the Morris water maze, showed higher levels of the Trx mRNA and protein in the hippocampus; apoptotic index of the neurons in the hippocampus of each group was negatively correlated with the Trx mRNA and protein levels. Conclusion The Trx deficit likely plays an important role in the impaired spatial learning and memory in the rats exposed to CIH and may work through the apoptosis of neurons in the hippocampus.展开更多
The stress-associated protein SAP12 belongs to the stress-associated protein （SAP） family with 14 members in Arabidopsis thaliana. SAP12 contains two AN1 zinc fingers and was identified in diagonal 2D redox SDS-PAGE...The stress-associated protein SAP12 belongs to the stress-associated protein （SAP） family with 14 members in Arabidopsis thaliana. SAP12 contains two AN1 zinc fingers and was identified in diagonal 2D redox SDS-PAGE as a protein undergoing major redox-dependent conformational changes. Its transcript was strongly induced under cold and salt stress in a time-dependent manner similar to SAP10, with high levels after 6 h and decreasing levels after 24 and 48 h. The tran- script regulation resembled those of the stress marker peroxiredoxin PrxllD at 24 and 48 h. Recombinant SAP12 protein showed redox-dependent changes in quaternary structure as visualized by altered electrophoretic mobility in non-reducing SDS polyacrylamide gel electrophoresis. The oxidized oligomer was reduced by high dithiothreitol concentrations, and also by E. coli thioredoxin TrxA with low dithiothreitol （DTF） concentrations or NADPH plus NADPH-dependent thioredoxin reductase. From Western blots, the SAP12 protein amount was estimated to be in the range of 0.5 ngμg^-1 leaf protein. SAP12 protein decreased under salt and cold stress. These data suggest a redox state-linked function of SAP12 in plant cells particularly under cold and salt stress.展开更多
Background Thioredoxin is one of the most important redox regulating proteins. Although thioredoxin has been shown to protect cells against different kinds of oxidative stress, the role of thioredoxin in myocardial is...Background Thioredoxin is one of the most important redox regulating proteins. Although thioredoxin has been shown to protect cells against different kinds of oxidative stress, the role of thioredoxin in myocardial ischemia and reperfusion injury has not been fully understood. This study was conducted to explore the protective role of human thioredoxin on myocardial ischemia and reperfusion injury and its potential mechanisms. Methods Purified human thioredoxin was injected into adult Wister rats, which were subjected to 30 minutes of myocardial ischemia followed by 2 or 24 hours of reperfusion. We detected 1） the infarct size; 2） the level of malondisldehyde （MDA） in serum; 3） the expression of caspase-9, and cytochrome c in/out of mitochondia by Western blotting; 4） apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling （TUNEL） assay and caspase-3 and its protein by reverse transcriptase polymerase chain reaction （RT-PCR） and Western blotting; 5） the expression of bcl-2 and bax in cardium by immunohistochemical （IHC） assay. Results Human thioredoxin reduced myocardial ischemia/reperfusion injury as evidenced by significant decrease of myocardial infarct size （P〈0.01）, notable reduction of myocyte apoptosis （P 〈0.01）, lower systemic oxidative stress level （P 〈0.01） after reperfusion for 2 hours, and few inflammatory cell infiltration after reperfusion for 24 hours in rats. Furthermore, treatment with human thioredoxin significantly reduced the release of mitochonddal cytochrome C （P〈0.05） and inhibited the activity of caspase-9 （P 〈0.05） and caspase-3 （P 〈0.01 in mRNA and P 〈0.05 at protein level）. Meanwhile, human thioredoxin markedly increased bcl-2 expression （P 〈0.05）. Conclusions These results strongly suggest that human thioredoxin has cardioprotective effects on myocardial ischemia/reperfusion and its anti-apoptotic role may be mediated by modulating bcl-2 and the mitochondria-dependent apoptotic signaling pathway展开更多
LHCII is a crucial light-harvesting pigment/protein complex in photosystem II (PSII) supercomplex. It also participates in the light energy redistribution between photosystems and in the photoprotection via its revers...LHCII is a crucial light-harvesting pigment/protein complex in photosystem II (PSII) supercomplex. It also participates in the light energy redistribution between photosystems and in the photoprotection via its reversible dissociation with PSII and PSI (photosystem I). This reversible detachment of LHCII is regulated by phosphorylation of its own and PSII core protein. Under low light conditions, LHCII is phosphorylated and dissociated with PSII core protein complex and combined with PSI, which balances the excitation energy between PSII and PSI;Under high light environment, the phosphorylation of PSII core proteins makes LHCII detach from PSII. The dissociated LHCII presents in a free state, which involves in the thermal dissipation of excess excitation energy. During photodamage, dual phosphorylations of both PSII core proteins and LHCII complexes occur. The phosphorylation of D1 is conductive to the disintegration of photodamaged PSII and the cycle of repair. In this circumstance, the phosphorylation of LHCII is induced by reactive oxygen species (ROS) and then the phosphorylated LHCII migrates to PSI, into the repair cycle of damaged PSII. The ferredoxin (Fdr) and thioredoxin (Tdr) system may play a possible central role in the phosphorylation regulation on LHCII dissociation.展开更多
文摘Vitamin D3 up-regulated protein 1 （VDUP1） is a multifunctional protein involved in maintaining cellular homeostasis. VDUP1 is induced by a variety of stresses. Inversely, VDUP1 is often reduced in various tumor tissues and cell lines. Over-expression of VDUP1 inhibits cell proliferation through cell cycle arrest. VDUP1 interacts with thioredoxin （Trx） and negatively regulates the expression and antioxidant function of Trx which is involved in redox regulation. VDUP1/ mice are more susceptible to carcinogenesis than wild-type mice and are defective in establishing immune system induding the development and function of natural killer cells. Furthermore, VDUP1^-/- mice show impaired Kreb cycle-mediated fatty acid utilization. In this review, we have discussed the multifunctional roles of VDUP1 in diverse cellular responses, in particular its relation to proliferation, apoptosis, differentiation, and diseases such as cancer and stress-related diseases.
文摘Reactive oxygen species (ROS) are produced under oxidative stress, such as high oxygen concentration and during the metabolic consumption of oxygen molecules. Male reproductive tissues appear to be continuously exposed to ROS produced by active metabolism. In addition, spermatozoa must pass through a high oxygen environment during the mating process. Thus, to maintain viable reproductive ability, a protective mechanism against oxidative stress is of importance. Here, we overview our current understanding of the cooperative function of antioxidative and redox systems that are involved in male fertility. Superoxide dismutase and glutathione peroxidase are major enzymes that scavenge harmful ROS in male reproductive organs. In turn, glutathione and thioredoxin systems constitute the main redox systems that repair oxidized and damaged molecules and also play a role in regulating a variety of cellular functions. While glutathione functions as an antioxidant by donating electrons to glutathione peroxidase and thioredoxin donates electrons to peroxiredoxin as a counterpart of glutathione peroxidase. In addition, aldo-keto reductases, which detoxify carbonyl compounds produced by oxidative stress, are present at high levels in the epithelia of the genital tract and Sertoli cells of the testis. Since these systems are involved in cross-talk, a comprehensive understanding will be required to maintain the physiological functions of male reproductive system.
文摘Sugarcane mosaic virus （SCMV） causes substantial losses of grain yield and forage biomass in susceptible maize worldwide. A major quantitative trait locus, Scmvl, has been identified to impart strong resistance to SCMV at the early infection stage. Here, we demonstrate that ZmTrxh, encoding an atypical h-type thioredoxin, is the causal gene at Scmvl, and that its transcript abundance correlated strongly with maize resistance to SCMV. ZmTrxh alleles, whether they are resistant or susceptible, share the identical coding/proximal promoter regions, but vary in the upstream regulatory regions. ZmTrxh lacks two canon- ical cysteines in the thioredoxin active-site motif and exists uniquely in the maize genome. Because of this, ZmTrxh is unable to reduce disulfide bridges but possesses a strong molecular chaperone-like activity. ZmTrxh is dispersed in maize cytoplasm to suppress SCMV viral RNA accumulation. Moreover, ZmTrxh- mediated maize resistance to SCMV showed no obvious correlation with the salicylic acid- and jasmonic acid-related defense signaling pathways. Taken together, our results indicate that ZmTrxh exhibits a distinct defense profile in maize resistance to SCMV, differing from previously characterized dominant or recessive potyvirus resistance genes.
基金This work was supported by a grant from the National Natural Science Foundation of China （No. 81070067）.
文摘Background Obstructive sleep apnea （OSA） can cause cognitive dysfunction and may be a reversible cause of cognitive loss in patients with Alzheimer＇s disease （AD）. Chronic exposure to intermittent hypoxia （IH）, such as encountered in OSA, is marked by neurodegenerative changes in rat brain. We investigated the change of thioredoxin （Trx）, spatial learning and memory in rats exposed to chronic intermittent hypoxia （CIH）. Methods Forty healthy male Sprague-Dawley （SD） rats were randomly divided into four groups of ten each： a CIH＋normal saline （CIH＋NS group）, a N-acetylcystein-treated CIH （CIH＋NAC） group, a sham CIH group （sham CIH＋NS）, and a sham NAC-treated sham CIH （CIH＋NAC） group. Spatial learning and memory in each group was assessed with the Morris water maze. Real-time PCR and Western blotting were used to examine mRNA and protein expression of Trx in the hippocampus tissue. The terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling （TUNEL） method was used to detect the apoptotic cells of the hippocampus CA1 region. Results CIH-rats showed impaired spatial learning and memory in the Morris water maze, including longer mean latencies for the target platform, reduced numbers of passes over the previous target platform and a smaller percentage of time spent in the target quadrant. Trx mRNA and protein levels were significantly decreased in the CIH-hippocampus, meanwhile, an elevated apoptotic index revealed apoptosis of hippocampal neurons of rats exposed to CIH. The rats, which acted better in the Morris water maze, showed higher levels of the Trx mRNA and protein in the hippocampus; apoptotic index of the neurons in the hippocampus of each group was negatively correlated with the Trx mRNA and protein levels. Conclusion The Trx deficit likely plays an important role in the impaired spatial learning and memory in the rats exposed to CIH and may work through the apoptosis of neurons in the hippocampus.
文摘The stress-associated protein SAP12 belongs to the stress-associated protein （SAP） family with 14 members in Arabidopsis thaliana. SAP12 contains two AN1 zinc fingers and was identified in diagonal 2D redox SDS-PAGE as a protein undergoing major redox-dependent conformational changes. Its transcript was strongly induced under cold and salt stress in a time-dependent manner similar to SAP10, with high levels after 6 h and decreasing levels after 24 and 48 h. The tran- script regulation resembled those of the stress marker peroxiredoxin PrxllD at 24 and 48 h. Recombinant SAP12 protein showed redox-dependent changes in quaternary structure as visualized by altered electrophoretic mobility in non-reducing SDS polyacrylamide gel electrophoresis. The oxidized oligomer was reduced by high dithiothreitol concentrations, and also by E. coli thioredoxin TrxA with low dithiothreitol （DTF） concentrations or NADPH plus NADPH-dependent thioredoxin reductase. From Western blots, the SAP12 protein amount was estimated to be in the range of 0.5 ngμg^-1 leaf protein. SAP12 protein decreased under salt and cold stress. These data suggest a redox state-linked function of SAP12 in plant cells particularly under cold and salt stress.
文摘Background Thioredoxin is one of the most important redox regulating proteins. Although thioredoxin has been shown to protect cells against different kinds of oxidative stress, the role of thioredoxin in myocardial ischemia and reperfusion injury has not been fully understood. This study was conducted to explore the protective role of human thioredoxin on myocardial ischemia and reperfusion injury and its potential mechanisms. Methods Purified human thioredoxin was injected into adult Wister rats, which were subjected to 30 minutes of myocardial ischemia followed by 2 or 24 hours of reperfusion. We detected 1） the infarct size; 2） the level of malondisldehyde （MDA） in serum; 3） the expression of caspase-9, and cytochrome c in/out of mitochondia by Western blotting; 4） apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling （TUNEL） assay and caspase-3 and its protein by reverse transcriptase polymerase chain reaction （RT-PCR） and Western blotting; 5） the expression of bcl-2 and bax in cardium by immunohistochemical （IHC） assay. Results Human thioredoxin reduced myocardial ischemia/reperfusion injury as evidenced by significant decrease of myocardial infarct size （P〈0.01）, notable reduction of myocyte apoptosis （P 〈0.01）, lower systemic oxidative stress level （P 〈0.01） after reperfusion for 2 hours, and few inflammatory cell infiltration after reperfusion for 24 hours in rats. Furthermore, treatment with human thioredoxin significantly reduced the release of mitochonddal cytochrome C （P〈0.05） and inhibited the activity of caspase-9 （P 〈0.05） and caspase-3 （P 〈0.01 in mRNA and P 〈0.05 at protein level）. Meanwhile, human thioredoxin markedly increased bcl-2 expression （P 〈0.05）. Conclusions These results strongly suggest that human thioredoxin has cardioprotective effects on myocardial ischemia/reperfusion and its anti-apoptotic role may be mediated by modulating bcl-2 and the mitochondria-dependent apoptotic signaling pathway
基金supported by the National Natural Science Foundation of China(No.30800399)Natural Science Foundation of Shanxi Province,China(No.2009011056-1)the Scientific Research Foundation for the Returned Overseas Chinese Scholars,Ministry of Education,China(No.2009-46)
文摘LHCII is a crucial light-harvesting pigment/protein complex in photosystem II (PSII) supercomplex. It also participates in the light energy redistribution between photosystems and in the photoprotection via its reversible dissociation with PSII and PSI (photosystem I). This reversible detachment of LHCII is regulated by phosphorylation of its own and PSII core protein. Under low light conditions, LHCII is phosphorylated and dissociated with PSII core protein complex and combined with PSI, which balances the excitation energy between PSII and PSI;Under high light environment, the phosphorylation of PSII core proteins makes LHCII detach from PSII. The dissociated LHCII presents in a free state, which involves in the thermal dissipation of excess excitation energy. During photodamage, dual phosphorylations of both PSII core proteins and LHCII complexes occur. The phosphorylation of D1 is conductive to the disintegration of photodamaged PSII and the cycle of repair. In this circumstance, the phosphorylation of LHCII is induced by reactive oxygen species (ROS) and then the phosphorylated LHCII migrates to PSI, into the repair cycle of damaged PSII. The ferredoxin (Fdr) and thioredoxin (Tdr) system may play a possible central role in the phosphorylation regulation on LHCII dissociation.
