Merck
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  • Enhanced cortical expression of myeloid differentiation primary response protein 88 (Myd88) in patients with traumatic brain injury.

Enhanced cortical expression of myeloid differentiation primary response protein 88 (Myd88) in patients with traumatic brain injury.

The Journal of surgical research (2012-11-29)
Wei Li, Huan-Dong Liu, Wan-Chun You, Meng-Liang Zhou, Hai-Ping Ling, Wei Shen, Lin Zhu, Chun-Hua Hang
摘要

Inflammatory response has been proven to play a crucial role in the pathophysilogical process after traumatic brain injury (TBI). Myeloid differentiation primary response protein 88 (Myd88) is considered as a vital factor for inflammation and immunity. Therefore, it is essential to know the detailed expression of Myd88 after TBI. However, the expression patterns of Myd88 in patients with TBI remain obscure. Hence, the aim of present study was to investigate the cortical expression of Myd88 in human contused brain. Nineteen contused brain tissue biopsies were obtained from 19 patients undergoing surgery for brain contusions 3 h-17 d after trauma, and samples of control group were from three patients in the pathway during surgical removal of deep benign tumors. The expression of Myd88 was assessed by quantitative real-time polymerase chain reaction, Western blotting, immunohistochemistry and double immunofluorescent staining, and the messenger RNA (mRNA) levels of tumor necrosis factor-alpha (TNF-α) and interleukin 1beta (IL-1β) were measured by quantitative real-time polymerase chain reaction. The progressively elevated mRNA and protein levels of Myd88 were detected after trauma, with the maximum after 72 h post-injury, and the distribution of Myd88 was found in neurons, astrocytes, and microglia. TNF-α and IL-1β mRNA levels ascended significantly within 12 h, and then descended gradually until after 72 h post-injury. Interestingly, there was a positive relationship between the expression of Myd88 and the proinflammatory cytokine TNF-α. These findings indicated that Myd88 might play an important role in the inflammatory response after human TBI.