Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice
Oxidative stress and glucose affect the expression of various genes that contribute to both reactive oxygen species generation and antioxidant systems. However, systemic alteration of oxidative stress-related gene expression in normal brains and in brains with a high-glucose status after ischemic–re...
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| Format: | Article |
| Language: | English |
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Elsevier
2012-05-01
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| Series: | Neurobiology of Disease |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0969996112000502 |
| _version_ | 1818350586526957568 |
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| author | Gab Seok Kim Joo Eun Jung Purnima Narasimhan Hiroyuki Sakata Pak H. Chan |
| author_facet | Gab Seok Kim Joo Eun Jung Purnima Narasimhan Hiroyuki Sakata Pak H. Chan |
| author_sort | Gab Seok Kim |
| collection | DOAJ |
| description | Oxidative stress and glucose affect the expression of various genes that contribute to both reactive oxygen species generation and antioxidant systems. However, systemic alteration of oxidative stress-related gene expression in normal brains and in brains with a high-glucose status after ischemic–reperfusion has not been explored. Using a polymerase chain reaction array system, we demonstrate that thioredoxin-interacting protein (Txnip) is induced by both oxidative stress and glucose. We found that Txnip mRNA is induced by ischemic–reperfusion injury and that Txnip is located in the cytoplasm of neurons. Moreover, in vitro oxygen–glucose deprivation (OGD) and subsequent reoxygenation without glucose and in vivo administration of 3-nitropropionic acid also promoted an increase in Txnip in a time-dependent manner, indicating that oxidative stress without glucose can induce Txnip expression in the brain. However, calcium channel blockers inhibit induction of Txnip after OGD and reoxygenation. Using the polymerase chain reaction array with ischemic and hyperglycemic-ischemic samples, we confirmed that enhanced expression of Txnip was observed in hyperglycemic-ischemic brains after middle cerebral artery occlusion. Finally, transfection of Txnip small interfering RNA into primary neurons reduced lactate dehydrogenase release after OGD and reoxygenation. This is the first report showing that Txnip expression is induced in neurons after oxidative or glucose stress under either ischemic or hyperglycemic-ischemic conditions, and that Txnip is proapoptotic under these conditions. |
| first_indexed | 2024-12-13T18:24:12Z |
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| id | doaj.art-bfbece36fab94949b6f6ad68fc6647e4 |
| institution | Directory Open Access Journal |
| issn | 1095-953X |
| language | English |
| last_indexed | 2024-12-13T18:24:12Z |
| publishDate | 2012-05-01 |
| publisher | Elsevier |
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| series | Neurobiology of Disease |
| spelling | doaj.art-bfbece36fab94949b6f6ad68fc6647e42022-12-21T23:35:38ZengElsevierNeurobiology of Disease1095-953X2012-05-01462440449Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in miceGab Seok Kim0Joo Eun Jung1Purnima Narasimhan2Hiroyuki Sakata3Pak H. Chan4Department of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USADepartment of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USADepartment of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USADepartment of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USACorresponding author at: Neurosurgical Laboratories, Stanford University, 1201 Welch Road, MSLS #P314, Stanford, CA 94305–5487, USA. Fax: +1 650 498 4550.; Department of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USAOxidative stress and glucose affect the expression of various genes that contribute to both reactive oxygen species generation and antioxidant systems. However, systemic alteration of oxidative stress-related gene expression in normal brains and in brains with a high-glucose status after ischemic–reperfusion has not been explored. Using a polymerase chain reaction array system, we demonstrate that thioredoxin-interacting protein (Txnip) is induced by both oxidative stress and glucose. We found that Txnip mRNA is induced by ischemic–reperfusion injury and that Txnip is located in the cytoplasm of neurons. Moreover, in vitro oxygen–glucose deprivation (OGD) and subsequent reoxygenation without glucose and in vivo administration of 3-nitropropionic acid also promoted an increase in Txnip in a time-dependent manner, indicating that oxidative stress without glucose can induce Txnip expression in the brain. However, calcium channel blockers inhibit induction of Txnip after OGD and reoxygenation. Using the polymerase chain reaction array with ischemic and hyperglycemic-ischemic samples, we confirmed that enhanced expression of Txnip was observed in hyperglycemic-ischemic brains after middle cerebral artery occlusion. Finally, transfection of Txnip small interfering RNA into primary neurons reduced lactate dehydrogenase release after OGD and reoxygenation. This is the first report showing that Txnip expression is induced in neurons after oxidative or glucose stress under either ischemic or hyperglycemic-ischemic conditions, and that Txnip is proapoptotic under these conditions.http://www.sciencedirect.com/science/article/pii/S0969996112000502Middle cerebral artery occlusionOxygen–glucose deprivationPolymerase chain reaction arrayReactive oxygen speciesThioredoxinThioredoxin-interacting protein |
| spellingShingle | Gab Seok Kim Joo Eun Jung Purnima Narasimhan Hiroyuki Sakata Pak H. Chan Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice Neurobiology of Disease Middle cerebral artery occlusion Oxygen–glucose deprivation Polymerase chain reaction array Reactive oxygen species Thioredoxin Thioredoxin-interacting protein |
| title | Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice |
| title_full | Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice |
| title_fullStr | Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice |
| title_full_unstemmed | Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice |
| title_short | Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice |
| title_sort | induction of thioredoxin interacting protein is mediated by oxidative stress calcium and glucose after brain injury in mice |
| topic | Middle cerebral artery occlusion Oxygen–glucose deprivation Polymerase chain reaction array Reactive oxygen species Thioredoxin Thioredoxin-interacting protein |
| url | http://www.sciencedirect.com/science/article/pii/S0969996112000502 |
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