Expression and cell distribution of myeloid differentiation primary response protein 88 in the cerebral cortex following experimental subarachnoid hemorrhage in rats: A pilot study

• Published in: Brain research Vol. 1520; pp. 134 - 144
• Main Authors: Sun, Qing, Dai, Yuxiang, Zhang, Xing, Hu, Yang-chun, Zhang, Dingding, Li, Wei, Zhang, Xiang-sheng, Zhu, Jian-hong, Zhou, Meng-liang, Hang, Chun-hua
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 03.07.2013; Elsevier
• Subjects: 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; 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
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2013.05.010

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.