Cytokine-mediated dysregulation of zonula occludens-1 properties in human brain microvascular endothelium

Rochfort, Keith D.; Cummins, Philip M.

doi:10.1016/j.mvr.2015.04.010

Cited by 83 publications

(53 citation statements)

References 22 publications

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“…Capaldo and Nusrat (2009) reported that the proinflammatory cytokines TNF-a, IL-1β and IL-8 regulated the expression of tight junction proteins. Studies showed that TNF-α decreases the mRNA expression level of ZO-1 in brain microvascular endothelial cells (Rochfort and Cummins 2015) and occludin in Caco-2 cells (Alsadi and Ma 2007). IL-8 reduced the level of mRNA encoding for ZO-1, claudin-5 and occludin in humans (Yu et al 2013).…”

Section: Discussionmentioning

confidence: 99%

A study of the damage of the intestinal mucosa barrier structure and function of Ctenopharyngodon idella with Aeromonas hydrophila

Kong

Chen

et al. 2017

Fish Physiol Biochem

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The aim of this study is to explore the effect of Aeromonas hydrophila on the intestinal mucosal barrier structure and intestinal permeability in grass carp (Ctenopharyngodon idella). Histopathological examinations showed that A. hydrophila induced severe intestinal lesions, including inflammatory cell infiltration and intestinal villus fusion and swelling. Messenger RNA (mRNA) expression of the inflammatory cytokines TNF-α, IL-1β, IL-8, IL-10 and MyD88 was significantly increased after infection with A. hydrophila. The permeability of intestinal mucosa was determined using Evans blue (EB) and D-lactic acid. The results indicated that the levels of EB and serum D-lactic acid were significantly increased after infection with A. hydrophila (p < 0.05). Our results also indicated that the intestinal mucosal barrier injury induced by A. hydrophila infection was closely associated with the expression of the tight junction (TJ) protein zonula occludens-1 (ZO-1), occludin, claudin b and claudin c as well as the activity of Na, K-ATPase and Ca, Mg-ATPase. Lower mRNA levels of occludin and lower Na, K-ATPase and Ca, Mg-ATPase activity in the intestines were observed after challenge. ZO-1 and claudin c were significantly increased 24 h after infection with A. hydrophila. The most interesting finding was that claudin b also significantly increased 24 h after challenge and then decreased to lower levels at 72, 120 and 168 h post-infection compared to the PBS-treated control group. The results demonstrated that grass carp infection with A. hydrophila induced intestinal inflammation and impaired the structure and function of the intestinal mucosal barrier.

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Section: Discussionmentioning

confidence: 99%

A study of the damage of the intestinal mucosa barrier structure and function of Ctenopharyngodon idella with Aeromonas hydrophila

Kong

Chen

et al. 2017

Fish Physiol Biochem

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“…For instance, one hallmark characteristic of sleep loss is the generation of a low-grade inflammatory status (reviewed in [31]). Several inflammatory mediators, such as the cytokines tumor necrosis factor (TFN)-α, interleukin (IL)-1β, IL-6, and IL-17A [32] as well as molecules such as C-reactive protein (CRP), cyclooxygenase (COX)-2, and endothelin (ET)-1 [4] are released during sleep loss and are able to modify tight junction protein expression both in in vitro and in in vivo experiments (for a review see [33, 34]). In addition, the decrease of ZO-1 and occludin might be associated to subtle permeability changes related to peripheral inflammation like that occurring in naturally aged rodents [35].…”

Section: Discussionmentioning

confidence: 99%

A2A Adenosine Receptor Antagonism Reverts the Blood-Brain Barrier Dysfunction Induced by Sleep Restriction

et al. 2016

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Chronic sleep restriction induces blood-brain barrier disruption and increases pro-inflammatory mediators in rodents. Those inflammatory mediators may modulate the blood-brain barrier and constitute a link between sleep loss and blood-brain barrier physiology. We propose that adenosine action on its A2A receptor may be modulating the blood-brain barrier dynamics in sleep-restricted rats. We administrated a selective A2A adenosine receptor antagonist (SCH58261) in sleep-restricted rats at the 10th day of sleep restriction and evaluated the blood-brain barrier permeability to dextrans coupled to fluorescein (FITC-dextrans) and Evans blue. In addition, we evaluated by western blot the expression of tight junction proteins (claudin-5, occludin, ZO-1), adherens junction protein (E-cadherin), A2A adenosine receptor, adenosine-synthesizing enzyme (CD73), and neuroinflammatory markers (Iba-1 and GFAP) in the cerebral cortex, hippocampus, basal nuclei and cerebellar vermis. Sleep restriction increased blood-brain barrier permeability to FITC-dextrans and Evans blue, and the effect was reverted by the administration of SCH58261 in almost all brain regions, excluding the cerebellum. Sleep restriction increased the expression of A2A adenosine receptor only in the hippocampus and basal nuclei without changing the expression of CD73 in all brain regions. Sleep restriction reduced the expression of tight junction proteins in all brain regions, except in the cerebellum; and SCH58261 restored the levels of tight junction proteins in the cortex, hippocampus and basal nuclei. Finally, sleep restriction induced GFAP and Iba-1 overexpression that was attenuated with the administration of SCH58261. These data suggest that the action of adenosine on its A2A receptor may have a crucial role in blood-brain barrier dysfunction during sleep loss probably by direct modulation of brain endothelial cell permeability or through a mechanism that involves gliosis with subsequent inflammation and increased blood-brain barrier permeability.

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“…111,112 Regarding BBB dysfunction, increased phosphorylation of ZO-1 on Tyr, Thr and Ser residues is associated with decreased ZO-1 expression and dissociation from the TJ complex during inflammation (TNF-a, IL-6, CCL2 or LPS treatment), hypoxia or ischemia through activation of PKC (cPKCa, nPKC-u and aPKC-z), Rho kinase p44/42 MAPK or p38MAPK/JNK pathways. 67,101,103,113,114 Similar to ZO-1, ZO-2 is regulated by Ser/Thr kinase activity (PKC, p44/ 42 MAPK or p38MAPK/JNK) and that phosphorylation may increase dissociation from the junction complex and increase permeability.…”

Section: Phosphorylationmentioning

confidence: 99%

Junctional proteins of the blood-brain barrier: New insights into function and dysfunction

et al. 2016

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Cytokine-mediated dysregulation of zonula occludens-1 properties in human brain microvascular endothelium

Cited by 83 publications

References 22 publications

A study of the damage of the intestinal mucosa barrier structure and function of Ctenopharyngodon idella with Aeromonas hydrophila

A study of the damage of the intestinal mucosa barrier structure and function of Ctenopharyngodon idella with Aeromonas hydrophila

A2A Adenosine Receptor Antagonism Reverts the Blood-Brain Barrier Dysfunction Induced by Sleep Restriction

Junctional proteins of the blood-brain barrier: New insights into function and dysfunction

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