scholarly journals MG53 permeates through blood-brain barrier to protect ischemic brain injury

Oncotarget ◽  
2016 ◽  
Vol 7 (16) ◽  
pp. 22474-22485 ◽  
Author(s):  
Yonggang Yao ◽  
Bo Zhang ◽  
Hua Zhu ◽  
Haichang Li ◽  
Yu Han ◽  
...  
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Blood Brain

scholarly journals Cystatin C improves blood–brain barrier integrity after ischemic brain injury in mice

2019 ◽  
Vol 153 (3) ◽  
pp. 413-425 ◽  
Author(s):  
Bo Yang ◽  
Junjie Xu ◽  
Liuhui Chang ◽  
Zhigang Miao ◽  
Dara Heang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Cystatin C ◽  
Brain Barrier ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Blood Brain Barrier Integrity

scholarly journals Endothelium‐targeted overexpression of Krüppel‐like factor 11 protects the blood‐brain barrier function after ischemic brain injury

2020 ◽  
Vol 30 (4) ◽  
pp. 746-765 ◽  
Author(s):  
Xuejing Zhang ◽  
Xuelian Tang ◽  
Feifei Ma ◽  
Yanbo Fan ◽  
Ping Sun ◽  
...  
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Barrier Function ◽  
Brain Barrier ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Blood Brain

scholarly journals Interleukin-1β Transfer across the Blood–Brain Barrier in the Ovine Fetus

2015 ◽  
Vol 35 (9) ◽  
pp. 1388-1395 ◽  
Author(s):  
Grazyna B Sadowska ◽  
Xiaodi Chen ◽  
Jiyong Zhang ◽  
Yow-Pin Lim ◽  
Erin E Cummings ◽  
...  
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Ischemia Reperfusion ◽  
Brain Regions ◽  
Interleukin 1Β ◽  
Brain Barrier ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Blood Brain ◽  
Hypoxic Ischemic Brain Injury

Pro-inflammatory cytokines contribute to hypoxic–ischemic brain injury. Blood–brain barrier (BBB) dysfunction represents an important component of hypoxic–ischemic brain injury in the fetus. Hypoxic–ischemic injury could accentuate systemic cytokine transfer across the fetal BBB. There has been considerable conjecture suggesting that systemic cytokines could cross the BBB during the perinatal period. Nonetheless, evidence to support this contention is sparse. We hypothesized that ischemia–reperfusion increases the transfer of systemic interleukin-1β (IL-1β) across the BBB in the fetus. Ovine fetuses at 127 days of gestation were studied 4 hours after 30 minutes of bilateral carotid artery occlusion and compared with a nonischemic group. Recombinant ovine IL-1β protein was expressed from an IL-1β pGEX-2 T vector in E. coli BL-21 cells and purified. The BBB function was quantified in 12 brain regions using a blood-to-brain transfer constant with intravenous 125I-radiolabeled IL-1β (125I-IL-1β). Interleukin-1β crossed the intact BBB in nonischemic fetuses. Blood-to-brain transport of 125I-IL-1β was higher ( P < 0.05) across brain regions in fetuses exposed to ischemia–reperfusion than nonischemic fetuses. We conclude that systemic IL-1β crosses the intact fetal BBB, and that ischemia–reperfusion increases transfer of this cytokine across the fetal BBB. Therefore, altered BBB function after hypoxia–ischemia facilitates entry of systemic cytokines into the brain of the fetus.

scholarly journals Ischemic-Reperfusion Injury Increases Matrix Metalloproteinases and Tissue Metalloproteinase Inhibitors in Fetal Sheep Brain

2018 ◽  
Vol 40 (3) ◽  
pp. 234-245 ◽  
Author(s):  
Xiaodi Chen ◽  
Aparna  Patra ◽  
Grazyna B. Sadowska ◽  
Barbara S. Stonestreet
Keyword(s):  
Brain Injury ◽  
Matrix Metalloproteinases ◽  
Protein Expression ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Ischemic Brain Injury ◽  
Fetal Sheep ◽  
Ischemic Brain ◽  
Blood Brain ◽  
Hypoxic Ischemic Brain Injury

Hypoxic-ischemic brain injury is a leading cause of neurodevelopmental morbidities in preterm and full-term infants. Blood-brain barrier dysfunction represents an important component of perinatal hypoxic-ischemic brain injury. The extracellular matrix (ECM) is a vital component of the blood-brain barrier. Matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) are important ECM components. They contribute to brain development, blood-brain barrier maintenance, and to regenerative and repair processes after hypoxic-ischemic brain injury. We hypothesized that ischemia at different durations of reperfusion affects the ECM protein composition of MMPs and TIMPs in the cerebral cortex of fetal sheep. Cerebral cortical samples were snap-frozen from sham control fetuses at 127 days of gestation and from fetuses after exposure to 30-min carotid occlusion and 4-, 24-, and 48-h of reperfusion. Protein expression of MMP-2, -8, -9, and -13 and TIMP-1, -2, -3, and -4 was measured by Western immunoblotting along with the gelatinolytic activity of MMP-2 and MMP-9 by zymography. The expression of MMP-8 was increased (Kruskal-Wallis, p = 0.04) in fetuses 48 h after ischemia. In contrast, changes were not observed in the protein expression of MMP-2, -9, or -13. The gelatinolytic activity of pro-MMP-2 was increased (ANOVA, p = 0.02, Tukey HSD, p = 0.05) 24 h after ischemia. TIMP-1 and -3 expression levels were also higher (TIMP-1, ANOVA, p = 0.003, Tukey HSD, p = 0.01; TIMP-3, ANOVA, p = 0.006, Tukey HSD, p = 0.01) 24 h after ischemia compared with both the sham controls and with fetuses exposed to 4 h of reperfusion. The changes in the expression of TIMP-1, -2, and -3 correlated with the changes in the MMP-8 and -13 protein expression. We speculate that regulation of MMP-8, MMP-13, and TIMPs contributes to ECM remodeling after is chemic-reperfusion injury in the fetal brain.

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