Nitric oxide plays a dual role in the oxidative injury of cultured rat microglia but not astroglia

Lee, C.-T.

doi:10.1016/j.neuroscience.2014.09.048

Cited by 14 publications

(13 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have reported that microglia become activated in OIR injury models [19] and from oxidative insults such as hydrogen peroxide (H 2 O 2 ) [42,43]. In the previous study, we have shown that H 2 O 2 level is increased in the retina in response to hyperoxia (P9), and is significantly reduced with MDL 72527 treatment [36].…”

Section: Resultsmentioning

confidence: 99%

“…In addition, blockade of PAO using MDL 72527 reduced OIR-induced increases in H 2 O 2 levels in the retina [36]. It is known that microglia cells are activated and their migration is enhanced by H 2 O 2 in vitro [42,43]. In the current study, we speculated that, in response to hyperoxia insult, PAO activation causes increased oxidative stress (through increases in H 2 O 2 levels) in retina leading to microglial activation, which would cause inflammation, slow the revascularization process and promote cell death.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Treatment with polyamine oxidase inhibitor reduces microglial activation and limits vascular injury in ischemic retinopathy

Patel

Shosha

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

Retinal vascular injury is a major cause of vision impairment in ischemic retinopathies. Insults such as hyperoxia, oxidative stress and inflammation contribute to this pathology. Previously, we showed that hyperoxia-induced retinal neurodegeneration is associated with increased polyamine oxidation. Here, we are studying the involvement of polyamine oxidases in hyperoxia-induced injury and death of retinal vascular endothelial cells. Newborn C57BL6/J mice were exposed to hyperoxia (70% O2) from postnatal day (P) 7 to 12 and were treated with the polyamine oxidase inhibitor MDL 72527 or vehicle starting at P6. Mice were sacrificed after different durations of hyperoxia and their retinas were analyzed to determine the effects on vascular injury, microglial cell activation, and inflammatory cytokine profiling. The results of this analysis showed that MDL 72527 treatment significantly reduced hyperoxia-induced retinal vascular injury and enhanced vascular sprouting as compared with the vehicle controls. These protective effects were correlated with significant decreases in microglial activation as well as levels of inflammatory cytokines and chemokines. In order to model the effects of polyamine oxidation in causing microglial activation in vitro, studies were performed using rat brain microvascular endothelial cells treated with conditioned-medium from rat retinal microglia stimulated with hydrogen peroxide. Conditioned-medium from activated microglial cultures induced cell stress signals and cell death in microvascular endothelial cells. These studies demonstrate the involvement of polyamine oxidases in hyperoxia-induced retinal vascular injury and retinal inflammation in ischemic retinopathy, through mechanisms involving cross-talk between endothelial cells and resident retinal microglia.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Treatment with polyamine oxidase inhibitor reduces microglial activation and limits vascular injury in ischemic retinopathy

Patel

Shosha

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

show abstract

“…NO may also activate p38 MAPK and p53 pathways, further increase DNA double strand breaks in microglia. However, the activation of both Akt and ERK cascades may alleviate the DNA damages induced by NO [ 22 ]. In diabetes and Alzheimer’s disease, the upregulates of NO synthase was also identified with the involved pathway of PPAR-γ, P38.…”

Section: No Overproductionmentioning

confidence: 99%

Cell toxicity mechanism and biomarker

Zhang

2018

Clinical & Translational Med

View full text Add to dashboard Cite

Cell toxicity may result in organ dysfunction and cause severe health problem. Recent studies revealed many toxicants may induced the over production of Nitric oxide, reactive oxygen species and the subsequent oxidative stress, cause cell toxicity. Mitochondrion dysfunction maybe the subsequent consequence of oxidative stress and has been recognized as another contributing factor in cell toxicity. Besides, oxidative products induced by some toxicants may also produce the compounds that damage cell DNA, leading to toxicity. Especially, the significance of nanoparticle induced cell toxicity was disclosed recently and attract more concern. The mechanism mainly includes inflammation, oxidative stress and DNA damage. On the other side, some biomarkers of cell toxicity including autophagy, cytokines, miRNA has been identified. The understanding of these phenomenon may enable us to clarify the cell toxicity mechanism then contribute to cell toxicity protection, disease treatment and drug side effect prevention.

show abstract

“…The two nNOS and eNOS enzymes are expressed primarily in mammalian cells and synthesize NO in response to increased levels of intracellular calcium [6]. When the heart is exposed to oxidative stress, NO is easily combined with reactive oxygen species, thereby forming nitrogen-reactive species [7]. NO also has harmful effects that are related to its oxidation products [8].…”

Section: Introductionmentioning

confidence: 99%

Effect of Hydroalcoholic Extract of Ribes khorasanicum on Acute Hypertension Induced by L-NAME in Rat

et al. 2019

View full text Add to dashboard Cite

Nitric oxide plays a dual role in the oxidative injury of cultured rat microglia but not astroglia

Cited by 14 publications

References 55 publications

Treatment with polyamine oxidase inhibitor reduces microglial activation and limits vascular injury in ischemic retinopathy

Treatment with polyamine oxidase inhibitor reduces microglial activation and limits vascular injury in ischemic retinopathy

Cell toxicity mechanism and biomarker

Effect of Hydroalcoholic Extract of Ribes khorasanicum on Acute Hypertension Induced by L-NAME in Rat

Contact Info

Product

Resources

About