Hydrogen peroxide-induced alterations of tight junction proteins in bovine brain microvascular endothelial cells

Lee, Heesang; Namkoong, Kee; Kim, Donghwa; Kim, Ki-Jeong; Cheong, Yoon-Hee; Kim, Sung‐Su; Lee, Won-Bok; Kim, Kyung-Yong

doi:10.1016/j.mvr.2004.07.005

Cited by 140 publications

(93 citation statements)

References 35 publications

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“…Hydroxyl radicals derived from superoxide anions have been reported as a key factor in increased vascular permeability produced by ischemia and systemic infusion or local superfusion of HX/XO (7,28,29 ] i and permeability indicate that these two ROS may trigger signaling pathways or evoke cellular damage via different cellular mechanisms. Currently, in vitro studies indicate that endothelial gap formation, the disruption of adhesion proteins, and the changes in cytoskeleton arrangements are the mechanisms for ROS-induced endothelial barrier dysfunction, which are similar to those reported in inflammatory mediator-induced permeability increases (1,9,12,17,20,21,36). Whether different cellular mechanisms are responsible for such distinct patterns of permeability increases in intact microvessels remains to be determined.…”

Section: Superoxide Induced Immediate and Transient Increases In Endomentioning

confidence: 63%

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Zhou¹,

Wen²,

Dong³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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He P. Calcium influxdependent differential actions of superoxide and hydrogen peroxide on microvessel permeability. Am J Physiol Heart Circ Physiol 296: H1096 -H1107, 2009. First published February 6, 2009 doi:10.1152/ajpheart.01037.2008.-Our previous study demonstrated that reactive oxygen species (ROS) released from activated blood cells contribute significantly to the increased microvessel permeability during inflammation. This study aims to define the individual roles of hydrogen peroxide (H 2O2) and superoxide in ROSinduced increases in permeability and endothelial intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) in individually perfused rat mesenteric venules. Microvessel permeability was determined by measuring hydraulic conductivity (L p). Endothelial [Ca 2ϩ ]i was measured in fura-2 AM-loaded microvessels. Perfusing microvessels with superoxide generated by hypoxanthine and xanthine oxidase (HX/XO) induced immediate and transient increases in L p. The mean peak value, which occurred within 5 min of HX/XO exposure, was 4.3 Ϯ 0.6 times that of the control. In contrast, the perfusion of H 2O2 (100 and 500 M) caused no immediate increases in L p. A significant Lp increase, 3.6 Ϯ 0.6 times the control value, occurred 30 min after the perfusion of H 2O2 at 500 M. The perfusion of H2O2 at 100 or 500 M for 1 h increased L p to 6.6 Ϯ 0.9 and 11.3 Ϯ 3.6 times the control value, respectively. The increased endothelial [Ca 2ϩ ]i in HX/XO or H 2O2 perfused vessels was correlated with the time course of the increases in L p. Inhibiting Ca 2ϩ influx by LaCl3 prevented the permeability increase induced by HX/XO or H 2O2. These results demonstrated differential actions of superoxide and H 2O2 on microvessel permeability and endothelial [Ca 2ϩ ]i. Superoxide-induced permeability increases were immediate and transient, whereas H 2O2-induced permeability increases were progressive, demonstrating concentration and time dependence. Ca 2ϩ influx plays an essential role in both superoxide and H 2O2-induced permeability increases. hydraulic conductivity; reactive oxygen species; endothelial calcium imaging REACTIVE OXYGEN species (ROS) contribute to various pathological conditions such as inflammation and ischemic reperfusion as well as atherosclerosis. A major source of ROS in the vascular system is from activated blood cells during respiratory burst. Our previous studies demonstrated that the ROS released from formyl Met-Leu-Phe-OH (fMLP)-stimulated neutrophils, either in suspension or from adherent leukocytes, cause immediate and transient increases in microvessel permeability (37,38). Prolonged permeability increases were observed with leukocyte/platelet aggregate adhesion to microvessel walls after initial endothelial cell activation by inflammatory mediators and endothelial gap formation (15). However, whether superoxide or hydrogen peroxide (H 2 O 2 ) converted from superoxide is the main species causing the increases in permeability under such experimental conditions remains unknown. Currently, most ROS-induced si...

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Section: Superoxide Induced Immediate and Transient Increases In Endomentioning

confidence: 63%

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Zhou¹,

Wen²,

Dong³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Although we did not identify the specific chemical nature of such pro-oxidant species, we can speculate that the effects are likely driven through different species. H 2 O 2 formation through Fenton's reaction is known to induce barrier leakage (Kim et al, 2008;Lee et al, 2004;Yamagata et al, 2004). However inhibition of H 2 O 2 by DFO (an iron chelator) was beneficial only under hypoxia.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, presence of oxidative stress has been associated with many neurological diseases including stroke, neurodegenerative diseases and traumatic brain injury (Freeman and Keller, 2012). Although oxidative stress is known to induce BBB breakdown or paracellular permeability (Clanton, 2005;Lee et al, 2004;Lochhead et al, 2010;Yamagata et al, 2004) its contribution to hypoxia-induced barrier breakdown remains unknown. In this study, we investigated the contribution of hypoxia-induced oxidative stress to barrier dysfunction in rat brain ECs.…”

Section: Introductionmentioning

confidence: 99%

Involvement of oxidative stress in hypoxia-induced blood–brain barrier breakdown

Ahmad

Gassmann

Ogunshola

2012

Microvascular Research

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The blood-brain barrier (BBB) is a cellular barrier formed by specialized brain endothelial cells under the influence of astrocytes and pericytes. Among the several stress factors known to induce BBB breakdown, hypoxia is probably the most represented but also the least understood. Recent evidence of oxidative stress occurring during hypoxia/ischemia situation raises its possible contribution to barrier breakdown. In this study, we investigated the relevance of oxidative stress in hypoxia-induced barrier disruption. Prolonged hypoxic exposure induced radical oxygen species (ROS) formation and induced glutathione oxidation. Such effects were accentuated under extreme O(2) deprived environment. Prooxidant treatment significantly disrupted barrier function under normal conditions, whereas anti-oxidant treatment contributed to maintain better barrier function and cell survival in an O(2)-reduced environment. In addition, the endothelial response to oxidative stress appeared modulated by the presence of astrocytes and pericytes, thus explaining some of the beneficial contribution of these cells as previously described. Taken together, this study highlights the importance of oxidative stress signaling at the barrier. In addition, cells of the neurovascular compartment differentially modulate ROS levels and also regulate barrier function. Thus, use of radical scavengers may be useful to support barrier function following stroke injury.

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“…The TJ consists of transmembrane proteins (occludin and claudins) that interact on adjacent endothelial cells to form a physical barrier to paracellular diffusion (Fanning et al, 1999) with accessory proteins such as ZO-1 and ZO-2 also playing an integral role (Anderson et al, 1995). Permeability changes have been correlated with alterations in expression and localization of ZO-1, claudin-5 and occludin ( (Brooks et al, 2006); (Huber et al, 2001a); (Lee et al, 2004)). In this study we examined the expression of ZO-1, occludin and claudin-5 under conditions of peripheral nerve block of CIP to help clarify the association between nociceptive input and changes in BBB integrity.…”

Section: Discussionmentioning

confidence: 99%

Nociceptive inhibition prevents inflammatory pain induced changes in the blood–brain barrier

et al. 2008

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Previous studies by our group have shown that peripheral inflammatory insult, using the λ-carrageenan inflammatory pain (CIP) model, induced alterations in the molecular and functional properties of the blood-brain barrier (BBB). The question remained whether these changes were mediated via an inflammatory and/or neuronal mechanism. In this study, we investigated the involvement of neuronal input from pain activity on alterations in BBB integrity by peripheral inhibition of nociceptive input. A perineural injection of 0.75% bupivacaine into the right hind leg prior to CIP was used for peripheral nerve block. Upon nerve block, there was a significant decrease in thermal allodynia induced by CIP, but no effect on edema formation 1 h post CIP. BBB permeability was increased 1 h post CIP treatment as determined by in situ brain perfusion of [ 14 C] sucrose; bupivacaine nerve block of CIP caused an attenuation of [ 14 C] sucrose permeability, back to saline control levels. Paralleling the changes in [ 14 C] sucrose permeability, we also report increased expression of three tight junction (TJ) proteins, zonula occluden-1 (ZO-1), occludin and claudin-5 with CIP. Upon bupivacaine nerve block, changes in expression were prevented. These data show that the λ-carrageenan induced changes in [ 14 C] sucrose permeability and protein expression of ZO-1, occludin and claudin-5 are prevented with inhibition of nociceptive input. Therefore, we suggest that nociceptive signaling is in part responsible for the alteration in BBB integrity under CIP.

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Hydrogen peroxide-induced alterations of tight junction proteins in bovine brain microvascular endothelial cells

Cited by 140 publications

References 35 publications

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Calcium influx-dependent differential actions of superoxide and hydrogen peroxide on microvessel permeability

Involvement of oxidative stress in hypoxia-induced blood–brain barrier breakdown

Nociceptive inhibition prevents inflammatory pain induced changes in the blood–brain barrier

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