NLRP3-dependent lipid droplet formation contributes to posthemorrhagic hydrocephalus by increasing the permeability of the blood–cerebrospinal fluid barrier in the choroid plexus

Zhang Zhaoqi; Guo Peiwen; Liang Liang; Jila Shiju; Ru Xufang; Zhang Qiang; Chen Jingyu; Chen Zhi; Feng Hua; Chen Yujie

doi:10.1038/s12276-023-00955-9

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자료유형: 학술저널

저자정보: Zhang Zhaoqi (Third Military Medical University (Army Medical University)) Guo Peiwen (Third Military Medical University (Army Medical University)) Liang Liang (Third Military Medical University (Army Medical University)) Jila Shiju (Third Military Medical University (Army Medical University)) Ru Xufang (Third Military Medical University (Army Medical University)) Zhang Qiang (Third Military Medical University (Army Medical University)) Chen Jingyu (Third Military Medical University (Army Medical University)) Chen Zhi (Third Military Medical University (Army Medical University)) Feng Hua (Third Military Medical University (Army Medical University)) Chen Yujie (Third Military Medical University (Army Medical University))

저널정보: 대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제55권

발행연도: 2023.3

수록면: 574 - 586 (13page)

DOI: 10.1038/s12276-023-00955-9

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Hydrocephalus is a severe complication that can result from intracerebral hemorrhage, especially if this hemorrhage extends into the ventricles. Our previous study indicated that the NLRP3 inflammasome mediates cerebrospinal fluid hypersecretion in the choroid plexus epithelium. However, the pathogenesis of posthemorrhagic hydrocephalus remains unclear, and therapeutic strategies for prevention and treatment are lacking. In this study, an Nlrp3−/− rat model of intracerebral hemorrhage with ventricular extension and primary choroid plexus epithelial cell culture were used to investigate the potential effects of NLRP3-dependent lipid droplet formation and its role in the pathogenesis of posthemorrhagic hydrocephalus. The data indicated that NLRP3-mediated dysfunction of the blood–cerebrospinal fluid barrier (B-CSFB) accelerated neurological deficits and hydrocephalus, at least in part, through the formation of lipid droplets in the choroid plexus; these lipid droplets interacted with mitochondria and increased the release of mitochondrial reactive oxygen species that destroyed tight junctions in the choroid plexus after intracerebral hemorrhage with ventricular extension. This study broadens the current understanding of the relationship among NLRP3, lipid droplets and the B-CSFB and provides a new therapeutic target for the treatment of posthemorrhagic hydrocephalus. Strategies to protect the B-CSFB may be effective therapeutic approaches for posthemorrhagic hydrocephalus.

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