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Reactive microglia and mitochondrial unfolded protein response following ventriculomegaly and behavior defects in kaolin-induced hydrocephalus
Jiebo Zhu 1,2,3,# (Graduate student), Min Joung Lee1,2,3,# (Research worker), Hee Jin Chang1,4 (Graduate student), Xianshu Ju1,3 (Research worker), Jianchen Cui1,3 (Graduate student), Yu Lim Lee1,3 (Graduate student), Dahyun Go1,2,3 (Graduate student), Woosuk Chung1,5,6 (Professor), Eungseok Oh1,4 (Professor), Junyoung Heo 1,2,3,* (Professor)
1Department of Medical Science and 2Department of Biochemistry and 3Infection Control Convergence Research Center, Chungnam National University School of Medicine,
4Department of Neurology, Chungnam National University Hospital,
5Department of Anesthesiology and Pain Medicine, Chungnam National University School of Medicine,
6Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital
Abstract
Ventriculomegaly induced by the abnormal accumulation of cerebrospinal fluid (CSF) leads to hydrocephalus, which is accompanied by neuroinflammation and mitochondrial oxidative stress. The mitochondrial stress activates mitochondrial unfolded protein response (UPRmt), which is essential for mitochondrial protein homeostasis. However, the association of inflammatory response and UPRmt in the pathogenesis of hydrocephalus is still unclear. To assess their relevance in the pathogenesis of hydrocephalus, we established a kaolin-induced hydrocephalus model in 8-week-old male C57BL/6J mice and evaluated it over time. We found that kaolin-injected mice showed prominent ventricular dilation, motor behavior defects at the 3-day, followed by the activation of microglia and UPRmt in the motor cortex at the 5-day. In addition, PARP-1/NF-リB signaling and apoptotic cell death appeared at the 5-day. Taken together, our findings demonstrate that activation of microglia and UPRmt occurs after hydrocephalic ventricular expansion and behavioral abnormalities which could be lead to apoptotic neuronal cell death, providing a new perspective on the pathogenic mechanism of hydrocephalus.
Abstract, Accepted Manuscript(in press) [Submitted on September 4, 2021, Accepted on December 4, 2021]
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