scholarly journals Histamine reduces ZO-1 tight-junction protein expression in cultured retinal microvascular endothelial cells

1996 ◽  
Vol 320 (3) ◽  
pp. 717-721 ◽  
Author(s):  
Thomas W. GARDNER ◽  
Treena LESHER ◽  
Sonny KHIN ◽  
Cuong VU ◽  
Alistair J. BARBER ◽  
...  

We examined ZO-1 protein content in cultured retinal vascular endothelial cells to test the hypothesis that histamine alters tight-junction-protein expression. Histamine (10-9 –10-4 M) causes a reversible concentration-dependent reduction of ZO-1 protein content, mediated by both H1 and H2 receptors. Histamine reduces ZO-1 expression within the time associated with increased paracellular permeability. Tight-junction-protein alterations may be a novel explanation for the mechanism by which vasoactive agents increase microvascular permeability.

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yi-Fang Tu ◽  
Si-Tse Jiang ◽  
Chi-Wu Chiang ◽  
Li-Ching Chen ◽  
Chao-Ching Huang

AbstractHypoxic-ischemic (HI) encephalopathy is the major cause of mortality and disability in newborns. The neurovascular unit is a major target of acute and chronic brain injury, and therapies that protect simultaneously both neurons and vascular endothelial cells from neonatal HI injury are in demand. Insulin receptors and its key downstream molecule-insulin receptor substrate −1 (IRS-1) are potential neuroprotective targets and expressed both in neuron and endothelial cells. To investigate whether IRS-1 can act similarly in neurons and vascular endothelial cells in protecting neurovascular units and brain form HI injury, we found that neuron-specific IRS-1 transgenic rats showed reduced neurovascular injury and infarct volumes, whereas endothelial-specific IRS-1 transgenic rats showed increased blood-brain barrier (BBB) disruption and exaggerated neurovascular injury after neonatal HI brain injury. Endothelial-specific IRS-1 overexpression increased vascular permeability and disassembled the tight junction protein (zonula occludens-1) complex. Inhibition of mammalian target of rapamycin (mTOR) by rapamycin preserved tight junction proteins and attenuated BBB leakage and neuronal apoptosis after HI in the endothelial-specific IRS-1 transgenic pups. Together, our findings suggested that neuronal and endothelial IRS-1 had opposite effects on the neurovascular integrity and damage after neonatal HI brain injury and that endothelial IRS-1 worsens neurovascular integrity after HI via mTOR-mediated tight junction protein disassembly.


2003 ◽  
Vol 74 (2) ◽  
pp. 255-265 ◽  
Author(s):  
Ibolya E. András ◽  
Hong Pu ◽  
Mária A. Deli ◽  
Avindra Nath ◽  
Bernhard Hennig ◽  
...  

2016 ◽  
Vol 84 (1) ◽  
pp. 99-101 ◽  
Author(s):  
Seon-Pil Jin ◽  
Sang Bum Han ◽  
Yeon Kyung Kim ◽  
Elizabeth Eunkyung Park ◽  
Eun Jin Doh ◽  
...  

2018 ◽  
Vol 9 (6) ◽  
pp. 3321-3329 ◽  
Author(s):  
H. Wu ◽  
T. Luo ◽  
Y. M. Li ◽  
Z. P. Gao ◽  
K. Q. Zhang ◽  
...  

Granny Smith apple procyanidin extracts upregulate tight junction protein expression, probably acting via the modulation of oxidative stress and inflammation in lipopolysaccharide-induced Caco-2 cells.


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