High-mobility group box-1 translocation and release after hypoxic ischemic brain injury in neonatal rats

被引：40

作者：

Chen, Xiaodi ^{[1
]}

Zhang, Jiyong ^{[1
]}

Kim, Boram ^{[1
]}

Jaitpal, Siddhant ^{[1
]}

Meng, Steven S. ^{[1
]}

Adjepong, Kwame ^{[1
]}

Imamura, Sayumi ^{[1
]}

Wake, Hidenori ^{[3
]}

Nishibori, Masahiro ^{[3
]}

Stopa, Edward G. ^{[2
]}

Stonestreet, Barbara S. ^{[1
]}

机构：

[1] Brown Univ, Dept Pediat, Alpert Med Sch, Women & Infants Hosp Rhode Isl, 101 Dudley St, Providence, RI 02905 USA

[2] Brown Univ, Rhode Isl Hosp, Alpert Med Sch, Dept Pathol & Neurosurg, Providence, RI 02903 USA

[3] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Okayama, Japan

来源：

EXPERIMENTAL NEUROLOGY | 2019年 / 311卷

基金：

美国国家卫生研究院;

关键词：

Brain; Hypoxia; HMGB1; Ischemia; Neonate; CHROMATIN PROTEIN HMGB1; TNF-ALPHA; CELLS; APOPTOSIS; AUTOPHAGY; NEURODEGENERATION; EXPRESSION; NEUROINFLAMMATION; ENCEPHALOPATHY; LOCALIZATION;

D O I：

10.1016/j.expneurol.2018.09.007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Inflammation contributes to neonatal brain injury. Pro-inflammatory cytokines represent key inflammatory meditators in neonatal hypoxic-ischemic (HI) brain injury. The high mobility group box-1 (HMGB1) protein is a nuclear protein with pro-inflammatory cytokine properties when it is translocated from the nucleus and released extracellularly after stroke in adult rodents. We have previously shown that HMGB1 is translocated from the nucleus to cytosolic compartment after ischemic brain injury in fetal sheep. In the current study, we utilized the Rice-Vannucci model to investigate the time course of HMGB1 translocation and release after HI injury in neonatal rats. HMGB1 was located in cellular nuclei of brains from sham control rats. Nuclear to cytoplasmic translocation of HMGB1 was detected in the ipsilateral-HI hemisphere as early as zero h after HI, and released extracellularly as early as 6 h after HI. Immunohistochemical double staining detected HMGB1 translocation mainly in neurons along with release from apoptotic cells after HI. Serum HMGB1 increased at 3 h and decreased by 24 h after HI. In addition, rat brains exposed to hypoxic injury alone also exhibited time dependent HMGB1 translocation at 3, 12 and 48 h after hypoxia. Consequently, HMGB1 responds similarly after HI injury in the brains of neonatal and adult subjects. We conclude that HMGB1 is sensitive early indicator of neonatal HI and hypoxic brain injury.

引用

页码：1 / 14

页数：14

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