Endothelin-1 Induces Production of the Neutrophil Chemotactic Factor Interleukin-8 by Human Brain-Derived Endothelial Cells

Increased levels of endothelin-1 (Et-1), a potent vasoconstrictor, have been correlated with hypertension and neuronal damage in ischemic/reperfusion injury. The presence of polymorphonuclear cells (PMNs) in the brain has been shown to be directly responsible for this observed pathology. To address the question of whether Et-1 plays a role in this process, human brain-derived endothelial cells (CNS-ECs) were cultured with Et-1. The results demonstrate that Et-1 induces production of the neutrophil chemoattractant interleukin-8 (IL-8) twofold to threefold after 72 hours; mRNA was maximal after 1 hour of stimulation. Conditioned culture medium derived from Et-1–stimulated CNS-ECs induced a chemotactic response in the PMN migration assay. The inflammatory cytokines tumor necrosis factor- (TNF) and IL-1β functioned additively with Et-1 in increasing IL-8 production. In contrast, transforming growth factor-β (TGF-β), but not IL-10, completely abolished the effect of Et-1 on IL-8 production. However, Et-1 did not modulate intercellular adhesion molecule-1 (ICAM-1) expression. These data demonstrate that Et-1 may be a risk factor in ischemic/reperfusion injury by inducing increased levels of the neutrophil chemoattractant IL-8. © 1998 by The American Society of Hematology.

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Endothelin-1 Induces Production of the Neutrophil Chemotactic Factor Interleukin-8 by Human Brain-Derived Endothelial Cells

Blood ◽

10.1182/blood.v92.9.3064 ◽

1998 ◽

Vol 92 (9) ◽

pp. 3064-3072 ◽

Cited By ~ 57

Author(s):

F.M. Hofman ◽

P. Chen ◽

R. Jeyaseelan ◽

F. Incardona ◽

M. Fisher ◽

...

Keyword(s):

Endothelial Cells ◽

Human Brain ◽

Reperfusion Injury ◽

Transforming Growth Factor ◽

Neuronal Damage ◽

Interleukin 8 ◽

Polymorphonuclear Cells ◽

Ischemic Reperfusion Injury ◽

Endothelin 1 ◽

Ischemic Reperfusion

Abstract Increased levels of endothelin-1 (Et-1), a potent vasoconstrictor, have been correlated with hypertension and neuronal damage in ischemic/reperfusion injury. The presence of polymorphonuclear cells (PMNs) in the brain has been shown to be directly responsible for this observed pathology. To address the question of whether Et-1 plays a role in this process, human brain-derived endothelial cells (CNS-ECs) were cultured with Et-1. The results demonstrate that Et-1 induces production of the neutrophil chemoattractant interleukin-8 (IL-8) twofold to threefold after 72 hours; mRNA was maximal after 1 hour of stimulation. Conditioned culture medium derived from Et-1–stimulated CNS-ECs induced a chemotactic response in the PMN migration assay. The inflammatory cytokines tumor necrosis factor- (TNF) and IL-1β functioned additively with Et-1 in increasing IL-8 production. In contrast, transforming growth factor-β (TGF-β), but not IL-10, completely abolished the effect of Et-1 on IL-8 production. However, Et-1 did not modulate intercellular adhesion molecule-1 (ICAM-1) expression. These data demonstrate that Et-1 may be a risk factor in ischemic/reperfusion injury by inducing increased levels of the neutrophil chemoattractant IL-8. © 1998 by The American Society of Hematology.

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Increased of heparanase expression in hypoxic/INS; endothelial cells and kidney ischemic-reperfusion injury associates with endothelin-1 elevation and eNOS reduction

Life Sciences ◽

10.1016/j.lfs.2013.12.077 ◽

2013 ◽

Vol 93 (25-26) ◽

pp. e17

Author(s):

Nur Arfian ◽

Keiko Yagi ◽

Kazuhiko Nakayama ◽

Dwi C. Ratna Sari ◽

Muhammad M. Romi ◽

...

Keyword(s):

Endothelial Cells ◽

Reperfusion Injury ◽

Ischemic Reperfusion Injury ◽

Endothelin 1 ◽

Ischemic Reperfusion

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Faculty Opinions recommendation of Progressive endothelin-1 gene activation initiates chronic/end-stage renal disease following experimental ischemic/reperfusion injury.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718012766.793479001 ◽

2013 ◽

Author(s):

Alejandro Chade

Keyword(s):

Renal Disease ◽

Reperfusion Injury ◽

End Stage Renal Disease ◽

Gene Activation ◽

Ischemic Reperfusion Injury ◽

Endothelin 1 ◽

Ischemic Reperfusion ◽

Stage Renal Disease ◽

End Stage

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Progressive endothelin-1 gene activation initiates chronic/end-stage renal disease following experimental ischemic/reperfusion injury

Kidney International ◽

10.1038/ki.2013.157 ◽

2013 ◽

Vol 84 (4) ◽

pp. 703-712 ◽

Cited By ~ 59

Author(s):

Richard A. Zager ◽

Ali C.M. Johnson ◽

Dennis Andress ◽

Kirsten Becker

Keyword(s):

Renal Disease ◽

Reperfusion Injury ◽

End Stage Renal Disease ◽

Gene Activation ◽

Ischemic Reperfusion Injury ◽

Endothelin 1 ◽

Ischemic Reperfusion ◽

Stage Renal Disease ◽

End Stage

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Long Non-coding RNA N1LR Protects Against Myocardial Ischemic/Reperfusion Injury Through Regulating the TGF-β Signaling Pathway

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.654969 ◽

2021 ◽

Vol 8 ◽

Author(s):

Lin Du ◽

Jie Chen ◽

Yong Wu ◽

Guangwei Xia ◽

Mingxing Chen ◽

...

Keyword(s):

Reperfusion Injury ◽

Signaling Pathway ◽

Protective Factor ◽

Transforming Growth Factor ◽

H9c2 Cell ◽

Cerebral Stroke ◽

Ischemic Reperfusion Injury ◽

Ischemic Reperfusion

Long non-coding RNAs (lncRNAs) have been shown to play critical roles in various cell biological processes. However, the mechanism of lncRNAs in acute myocardial infarction (AMI) is not fully understood. Previous studies showed that lncRNA N1LR was down-regulated in ischemic cerebral stroke and its up-regulation was protective. The current study was designed to assess the protective effect of N1LR and further to explore potential mechanisms of N1LR in ischemic/reperfusion (I/R) injury after AMI. Male C57BL/6J mice and H9c2 cardiomyocytes were selected to construct in vivo and in vitro pathological models. In H9c2 cell line, N1LR expression was markedly decreased after H2O2 and CoCl2 treatments and N1LR overexpression alleviated apoptosis, inflammation reaction, and LDH release in cardiomyocytes treated with H2O2 and CoCl2. Mouse in vivo study showed that overexpression of N1LR enhanced cardiac function and suppressed inflammatory response and fibrosis. Mechanistically, we found that the expression of transforming growth factor (TGF)-β1 and smads were significantly decreased in the N1LR overexpression group exposed to H2O2. In a summary, our study indicated that N1LR can act as a protective factor against cardiac ischemic-reperfusion injury through regulating the TGF-β/Smads signaling pathway.

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Repression of adenosine triphosphate–binding cassette transporter ABCG2 by estrogen increases intracellular glutathione in brain endothelial cells following ischemic reperfusion injury

Neurobiology of Aging ◽

10.1016/j.neurobiolaging.2018.02.020 ◽

2018 ◽

Vol 66 ◽

pp. 138-148 ◽

Cited By ~ 5

Author(s):

Jin A. Shin ◽

Sae Im Jeong ◽

Hye Won Kim ◽

Gyeonghui Jang ◽

Dong-Ryeol Ryu ◽

...

Keyword(s):

Endothelial Cells ◽

Reperfusion Injury ◽

Adenosine Triphosphate ◽

Brain Endothelial Cells ◽

Ischemic Reperfusion Injury ◽

Ischemic Reperfusion ◽

Intracellular Glutathione

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Faculty Opinions recommendation of Progressive endothelin-1 gene activation initiates chronic/end-stage renal disease following experimental ischemic/reperfusion injury.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718012766.793480648 ◽

2013 ◽

Author(s):

David Pollock

Keyword(s):

Renal Disease ◽

Reperfusion Injury ◽

End Stage Renal Disease ◽

Gene Activation ◽

Ischemic Reperfusion Injury ◽

Endothelin 1 ◽

Ischemic Reperfusion ◽

Stage Renal Disease ◽

End Stage

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Effects of allopurinol on smoke inhalation in the ovine model

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.1.228 ◽

1990 ◽

Vol 68 (1) ◽

pp. 228-234 ◽

Cited By ~ 10

Author(s):

S. Y. Ahn ◽

K. Sugi ◽

P. Talke ◽

J. L. Theissen ◽

H. A. Linares ◽

...

Keyword(s):

Reperfusion Injury ◽

Smoke Inhalation ◽

Polymorphonuclear Cells ◽

Ovine Model ◽

Lung Water ◽

Ischemic Reperfusion Injury ◽

Xanthine Oxidase Inhibitor ◽

Ischemic Reperfusion ◽

Significant Difference ◽

Pulmonary Damage

We hypothesized that the pulmonary damage induced by smoke inhalation is the result of ischemic reperfusion injury. We determined the effect of allopurinol (xanthine oxidase inhibitor) on the pulmonary microvascular fluid flux in an ovine model after inhalation of cotton smoke (n = 13) and compared these data with those from untreated similarly smoke-injured (n = 7), as well as sham- (air, n = 9) smoked, animals and sheep given an equivalent dose of CO (n = 7). Smoke injury resulted in an increased lung lymph flow, lymph-to-plasma protein ratio, lung content of polymorphonuclear cells, and extravascular lung water (gravametric), in addition to histological evidence of tissue (pulmonary) edema and destruction. No significant difference was found in these variables between the sheep that were injured with smoke whether or not they were pretreated with allopurinol. The sham-smoked and CO-insufflated animals showed no significant changes in cardiopulmonary function or morphology. We conclude that there are few data to support a role of ischemic reperfusion injury in the pulmonary damage seen after smoke inhalation.

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