Reduction by NG‐nitro‐L‐arginine of H2O2‐induced endothelial cell injury

Shimizu, Shunichi; Nomoto, Masaki; Yamamoto, Toshinori; Momose, Kazutaka

doi:10.1111/j.1476-5381.1994.tb17026.x

Cited by 35 publications

(19 citation statements)

References 29 publications

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“…We previously reported that L-NAME, but not L-NMA, attenuates the external H202-induced endothelial cell injury, although both completely inhibited nitric oxide synthesis (Shimizu et al 1994). Interestingly, nitric oxide synthase has been shown to release reactive oxygen species in the presence of low concentrations of tetrahydrobiopterin, a cofactor of nitric oxide synthase, or L-arginine, a substrate of nitric oxide synthase (Heinzel et al 1992;Pou et al 1992).…”

Section: Discussionmentioning

confidence: 99%

“…Bovine aortic endothelial cells were cultured as previously described (Shimizu et al 1994). Fresh bovine thoracic aortae obtained from an abattoir were kept in ice-cold phosphatebuffered saline solufion containing 100 U/ml penicillin and 100 pg/ml streptomycin.…”

Section: Methodsmentioning

confidence: 99%

“…Cell injury was estimated by determination of leakage of lactate dehydrogenase as previously described (Shimizu et al 1994). Confluent endothelial or rat foetal lung fibroblast cells in 24-well plates were washed three times with Krebs solution @H 7.4) containing 118.5 mM NaCl, 4.74 mM KC1, 2.5 mM CaC12.…”

Section: Methodsmentioning

confidence: 99%

“…cell injury, but not NG-methyl-L-arginine, also an inhibitor of nitric oxide synthase (Shimizu et al 1994). L-NAME has been shown to block the generation of reactive oxygen species from nitric oxide synthase, whereas NG-methyl-L-arginine has no effect on this reaction (Heinzel et al 1992;Pou et al 1992).…”

Section: -5-8mentioning

confidence: 99%

“…L-NAME has been shown to block the generation of reactive oxygen species from nitric oxide synthase, whereas NG-methyl-L-arginine has no effect on this reaction (Heinzel et al 1992;Pou et al 1992). Therefore, we speculated that L-NAME may inhibit reactive oxygen species production from nitric oxide synthase during H202 treatment, and may attenuate H202-induced endothelial cell injury (Shimizu et al 1994).…”

Section: -5-8mentioning

confidence: 99%

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Possible Involvement of Nitric Oxide Synthase in Oxidative Stress‐Induced Endothelial Cell Injury

Ishii

Yamamoto

Shimizu

et al. 1997

Pharmacology & Toxicology

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Abstract:The purpose of this study was to characterize the protective effect of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, on oxidative stress-induced endothelial cell injury. Intracellular oxidative stresi was induced by I -chloro-2,4-dinitrobenzene, a glutathione (GSH) depleting agent, and the leakage of intracellular lactate dehydrogenase was measured as a marker of cell injury. Addition of 1 -chloro-2,4-dinitrobenzene (100-500 pM) induced leakage of lactate dehydrogenase from endothelial cells, and the leakage of lactate dehydrogenase was strongly attenuated by L-NAME, but not by NG-methyl-L-arginine, also an inhibitor of nitric oxide synthase. However, cell injury induced by the Ca2+ ionophore ionomycin was not affected by L-NAME or NG-methyl-L-arginine. Moreover, neither L-NAME nor NG-methyl-L-arginine affected GSH depleting agent-induced or H202-induced cell injury in a rat foetal lung fibroblast cell line which lacks nitric oxide synthase. These results suggest that the protective effect of L-NAME is likely to be related to nitric oxide synthase, while the inhibition of nitric oxide production may not be involved in the protective effect of L-NAME, since NG-methyl-L-arginine did not affect endothelial cell injury.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: -5-8mentioning

confidence: 99%

Section: -5-8mentioning

confidence: 99%

See 3 more Smart Citations

Possible Involvement of Nitric Oxide Synthase in Oxidative Stress‐Induced Endothelial Cell Injury

Ishii

Yamamoto

Shimizu

et al. 1997

Pharmacology & Toxicology

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Keap1‐Nrf2 signaling pathway in angiogenesis and vascular diseases

Guo

Zhang

2020

J Tissue Eng Regen Med

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The transcription factor, nuclear factor E2-related factor 2 (Nrf2), is highly sensitive to oxidative burst products, including reactive oxygen species (ROS) and reactive nitrogen species. In the cell nucleus, Nrf2 activates various antioxidant genes by binding to the antioxidant response elements. As an adapter for cullin 3/ring-box 1, kelch-like ECH-associated protein 1 (Keap1) ubiquitinates and degrades Nrf2 under physiological conditions. Conversely, with the aggravation of oxidative stress, Keap1-Nrf2 interaction could be much more easily dissociated. ROS play a key role in regulating the redox signaling pathway and affect the vasculature in a dosedependent manner. Long-term production or high concentration of ROS are harmful to the vascular system, while moderate ROS can promote angiogenesis and tissue regeneration. Furthermore, appropriate regulation of oxidative stress mediated via the Keap1-Nrf2 pathway would be beneficial in various diseases associated with abnormal angiogenesis, including diabetes and cancers. Nrf2 deficiency has also been shown to result in significantly impaired survival, proliferation, and angiogenic capacity of endothelial cells in a hind limb ischemia model. Thus, this review will briefly summarize the underlying molecular mechanisms of Keap1-Nrf2 pathway in regulating oxidative stress and also help elucidate the critical role of Keap1-Nrf2 in angiogenesis under physiological and pathological conditions. K E Y W O R D S angiogenesis, diabetes, endothelial cells, Keap1/Nrf2, ROS, tumors

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