Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: A pilot study
Abstract Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and t...
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Published in | Brain research Vol. 1520; pp. 134 - 144 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier B.V
03.07.2013
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Abstract | Abstract Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF-κB and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2 h, 6 h, 12 h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3 ml autoblood into the prechiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF-α and IL-1β were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1β, there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. |
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AbstractList | Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF-κB and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2h, 6h, 12h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3 ml autoblood into the prechiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF-α and IL-1β were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1β, there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF-κB and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2h, 6h, 12h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3ml autoblood into the prechiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF-α and IL-1β were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1β, there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. •We detect expression of MyD88 in experimental model of SAH.•MyD88 features a biphasic expression similar to IL-1β expression after SAH.•Over-expressed MyD88 is mainly located in neurons.•Neuronal MyD88 might be involved in the inflammatory response after SAH. Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF- Kappa B), Interleukin 1 beta (IL-1 beta ) and tumor necrosis factor- alpha (TNF- alpha ) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF- Kappa B and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2h, 6h, 12h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3ml autoblood into the prechiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF- alpha and IL-1 beta were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1 beta , there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF-κB and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2h, 6h, 12h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3ml autoblood into the prechiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF-α and IL-1β were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1β, there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. Abstract Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation contributes to the poor outcome caused by SAH. Toll like receptors (TLRs), nuclear factor-kappaB (NF-κB), Interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the damaging inflammation process after SAH. Myeloid differentiation primary response protein 88 (MyD88) is essential to deliver TLRs signals down to NF-κB and pro-inflammatory factors. The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after SAH. Sprague Dawley (SD) rats were randomly divided into sham group and SAH groups at 2 h, 6 h, 12 h and on day 1, day 2, day 3, day 5 and day 7. SAH groups suffered experimental subarachnoid hemorrhage by injection of 0.3 ml autoblood into the prechiasmatic cistern. MyD88 expression is measured by western blot analysis, real-time polymerase chain reaction (PCR), immunohistochemistry and immunofluorescence. The levels of TNF-α and IL-1β were measured by real-time PCR. Our results demonstrated MyD88 expression was increased after SAH, and peaked on day 1 and day 5, which showed a parallel time course to the up-regulation of IL-1β, there was a highly positive relationship between them. Immunohistochemistry and immunofluorescence results indicated up-regulated MyD88 was mainly located in neurons while over expressed MyD88 could also be found in astrocytes and microglia. These results might have important implications during the administration of specific MyD88 antagonists in order to prevent or reduce inflammatory response following SAH. |
Author | Dai, Yuxiang Sun, Qing Hu, Yang-chun Zhou, Meng-liang Zhang, Xing Hang, Chun-hua Zhu, Jian-hong Li, Wei Zhang, Dingding Zhang, Xiang-sheng |
Author_xml | – sequence: 1 fullname: Sun, Qing – sequence: 2 fullname: Dai, Yuxiang – sequence: 3 fullname: Zhang, Xing – sequence: 4 fullname: Hu, Yang-chun – sequence: 5 fullname: Zhang, Dingding – sequence: 6 fullname: Li, Wei – sequence: 7 fullname: Zhang, Xiang-sheng – sequence: 8 fullname: Zhu, Jian-hong – sequence: 9 fullname: Zhou, Meng-liang – sequence: 10 fullname: Hang, Chun-hua |
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Keywords | IL-1 receptor associated kinase CPP BBB Toll like receptors CNS Iba1 MyD88 Myeloid differentiation primary response protein 88 NF-κB Inflammatory cytokine inhibitor of nuclear factor kappa-B kinase neunron-specific nuclear protein IKK Interleukin 1β IL-1β central nervous system GFAP blood brain barrier IRAK NeuN intracranial pressure subarachnoid hemorrhage ICP nuclear factor-kappaB SAH glial fibrillary acidic protein TLRs ionized calcium binding adapter molecule 1 cerebral perfusion pressure Subarachnoid hemorrhage Human Cerebral cortex Rat Response differentiation Rodentia Central nervous system Cytokine Cardiovascular disease Inflammation Gene expression Protein Encephalon Myeloid differentiation primary Vertebrata Mammalia response protein 88 Animal Distribution |
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Snippet | Abstract Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that... Subarachnoid hemorrhage (SAH) which is mostly caused by aneurysm rupture causes a lot of death every year. Convincing evidence can be made that inflammation... |
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SubjectTerms | aneurysm Animals antagonists astrocytes Biological and medical sciences Blotting, Western cerebral cortex Cerebral Cortex - metabolism death Disease Models, Animal Fluorescent Antibody Technique hemorrhage Immunohistochemistry inflammation Inflammatory cytokine interleukins Male Medical sciences Myeloid Differentiation Factor 88 - analysis Myeloid Differentiation Factor 88 - metabolism Myeloid differentiation primary response protein 88 necrosis Neurology neurons Pilot Projects quantitative polymerase chain reaction Rats Rats, Sprague-Dawley Real-Time Polymerase Chain Reaction receptors Subarachnoid hemorrhage Subarachnoid Hemorrhage - metabolism Vascular diseases and vascular malformations of the nervous system Western blotting |
Title | Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: A pilot study |
URI | https://www.clinicalkey.es/playcontent/1-s2.0-S0006899313006550 https://dx.doi.org/10.1016/j.brainres.2013.05.010 https://www.ncbi.nlm.nih.gov/pubmed/23684713 https://search.proquest.com/docview/1369233387 https://search.proquest.com/docview/1660411825 |
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