Carbon monoxide blocks oxidative stress-induced hepatocyte apoptosis via inhibition of the p54 JNK isoform

Rosa, Laura Conde de la; Vrenken, Titia E.; Hannivoort, Rebekka A.; Buist‐Homan, Manon; Havinga, Rick; Slebos, Dirk‐Jan; Kauffman, Henk F.; Faber, Klaas Nico; Jansen, Peter; Moshage, Han

doi:10.1016/j.freeradbiomed.2007.12.011

Cited by 45 publications

(48 citation statements)

References 48 publications

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“…HO cleaves the α-meso carbon bridge of heme, yielding equimolar quantities of carbon monoxide (CO), Fe 2+ ions, and biliverdin. 15,16) The overexpression of HO-1 has been reported to augment apoptosis in breast cancer 17) and astroglia, 18) and our present data support a facilitatory role of HO-1 in apoptosis. Alternatively, the anti-apoptotic effects of HO-1 have been reported colon cancer, 19) thyroid cancer, 20) and gastric cancer.…”

Section: Discussionsupporting

confidence: 83%

Vitamin K3 Analogs Induce Selective Tumor Cytotoxicity in Neuroblastoma

Kitano

Yoda

Tabata

et al. 2012

Biological & Pharmaceutical Bulletin

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Section: Discussionsupporting

confidence: 83%

Vitamin K3 Analogs Induce Selective Tumor Cytotoxicity in Neuroblastoma

Kitano

Yoda

Tabata

et al. 2012

Biological & Pharmaceutical Bulletin

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“…Previous observations in cultured hepatocytes suggested that JNK activation is involved in superoxide-induced apoptosis (11,12,44). To verify these findings in the intact liver, the levels of c-Jun and phospho-c-Jun were evaluated after diquat treatment.…”

Section: Resultsmentioning

confidence: 91%

“…Menadione caused apoptosis through activation of the c-Jun NH 2 -terminal kinase (JNK) and AP-1 in RALA255 cells (15). In contrast to these findings, only the superoxide-generating chemicals menadione and paraquat caused caspase-and JNK-dependent apoptotic cell death in primary rat hepatocytes (11,12). H 2 O 2 did activate neither JNK nor caspases and induced necrosis in rat hepatocytes (11).…”

mentioning

confidence: 96%

Oxidant stress-induced liver injury in vivo: role of apoptosis, oncotic necrosis, and c-Jun NH₂-terminal kinase activation

Hong¹,

Lebofsky²,

Farhood³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Hong JY, Lebofsky M, Farhood A, Jaeschke H. Oxidant stressinduced liver injury in vivo: role of apoptosis, oncotic necrosis, and c-Jun NH2-terminal kinase activation. Am J Physiol Gastrointest Liver Physiol 296: G572-G581, 2009. First published January 8, 2009 doi:10.1152/ajpgi.90435.2008.-Oxidant stress is critically involved in various liver diseases. Superoxide formation causes c-Jun NH2-terminal kinase (JNK)-and caspase-dependent apoptosis in cultured hepatocytes. To verify these findings in vivo, male Fisher rats were treated with diquat and menadione. The oxidant stress induced by both compounds was confirmed by increased formation of glutathione disulfide and 4-hydroxynonenal protein adducts. Plasma alanine aminotransferase activities increased from 46 Ϯ 4 U/l in controls to 955 Ϯ 90 U/l at 6 h after diquat treatment. Hematoxylin and eosin staining of liver sections revealed large areas of necrotic cells at 3 and 6 h. DNA strandbreaks, evaluated with the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay, showed clusters of TUNEL-positive cells, where the staining was predominantly cytosolic and the cells were swollen, indicating oncotic necrosis. There was no significant increase in caspase-3 activities or relevant release of DNA fragments into the cytosol at any time between 0 and 6 h after diquat treatment. Despite the activation of JNK after high doses of diquat, the JNK inhibitor SP-600125 did not protect against diquat-induced necrosis. Menadione alone did not cause liver injury, but, in combination with phorone and FeSO4, induced moderate oncotic necrosis. On the other hand, if animals were treated with galactosamine/endotoxin as positive control for apoptosis, caspase-3 activities were increased by 259%, the number of TUNEL-positive cells with apoptotic morphology was increased 103-fold, and DNA fragmentation was enhanced 6-fold. The data indicate that liver cell death initiated by diquat-induced superoxide formation in vivo is mediated predominantly by oncotic necrosis and is independent of JNK activation.

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“…In addition to the above mentioned strategies for attenuating oxidative stress, inhibitors blocking Tiam1/Rac1/Nox signaling axis, 57,94,106 polyphenolic extracts supplementation, 107 stress activated kinase inhibitors, [108][109][110][111] and angiotensin receptor antagonists 112 have proven efficaciously to reduce oxidative stress and improve islet β-cell function.…”

Section: Potential Therapeutic Targets and Interventional Modalitiesmentioning

confidence: 99%

Biphasic Roles of a Small G-Protein, RAC1 in Pancreatic Β-Cell

Parmar¹,

Meer²,

Syed³

2015

Gastro Open J

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Glucose-stimulated insulin secretion (GSIS) involves cross talk between small Gproteins and their regulating factors. These interactions results in translocation of insulin-laden granules to the plasma membrane for fusion and insulin release. Vesicular transport and fusion events are tightly regulated by signals which coordinate between vesicle-and membrane-associated docking proteins. It is now being accepted that small G-protein, Rac1-mediated Reactive Oxygen Species (ROS) functions as a second messenger in islet β-cell function. Further, evidence from multiple laboratories suggests a tonic increase in ROS generation is necessary for GSIS and fatty acid-induced insulin secretion. On the other hand, Rac1-mediated NADPH oxidase-activation and subsequent generation of excessive ROS under glucolipotoxic conditions and cytokines exposure has proven to be detrimental for islet β-cell function. In this review we overview the normal physiological effects (positive role) and adverse effects (negative role) of activated small G-protein, Rac1 in pancreatic β-cells.

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Carbon monoxide blocks oxidative stress-induced hepatocyte apoptosis via inhibition of the p54 JNK isoform

Cited by 45 publications

References 48 publications

Vitamin K3 Analogs Induce Selective Tumor Cytotoxicity in Neuroblastoma

Vitamin K3 Analogs Induce Selective Tumor Cytotoxicity in Neuroblastoma

Oxidant stress-induced liver injury in vivo: role of apoptosis, oncotic necrosis, and c-Jun NH₂-terminal kinase activation

Biphasic Roles of a Small G-Protein, RAC1 in Pancreatic Β-Cell

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Carbon monoxide blocks oxidative stress-induced hepatocyte apoptosis via inhibition of the p54 JNK isoform

Cited by 45 publications

References 48 publications

Vitamin K3 Analogs Induce Selective Tumor Cytotoxicity in Neuroblastoma

Vitamin K3 Analogs Induce Selective Tumor Cytotoxicity in Neuroblastoma

Oxidant stress-induced liver injury in vivo: role of apoptosis, oncotic necrosis, and c-Jun NH2-terminal kinase activation

Biphasic Roles of a Small G-Protein, RAC1 in Pancreatic Β-Cell

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Oxidant stress-induced liver injury in vivo: role of apoptosis, oncotic necrosis, and c-Jun NH₂-terminal kinase activation