Expression of endothelial nitric oxide synthase in the ischemic penumbra: relationship to expression of neuronal nitric oxide synthase and vascular endothelial growth factor

Leker, Ronen R.; Teichner, Angella; Ovadia, Haim; Keshet, Eli; Reinherz, Esther; Ben‐Hur, Tamir

doi:10.1016/s0006-8993(01)02561-6

Cited by 54 publications

(33 citation statements)

References 37 publications

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“…These changes in 2VO-induced expression of angiogenic molecules, VEGF and bFGF, might possibly indicate that SNO-PEG-Hb prevented the progression of ischemia-induced cerebrovascular remodeling in the hippocampus. Of note is that eNOS and VEGF expression patterns dissociated in the hippocampus of 2VO rats with SNO-PEG-Hb treatment, although the similarity of anatomical and temporal pattern of VEGF and eNOS induction has been reported in the rat brain with permanent ischemia (44). Very recently, reciprocal regulation between NO and VEGF has been reported (45 -47): exogenous NO significantly enhanced angiogenesis in the ischemic brain with a concomitant increase in VEGF levels, while an excessive amount of NO negatively controlled VEGF synthesis.…”

Section: Discussionmentioning

confidence: 88%

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

et al. 2004

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Abstract. Evidence suggests that S-nitrosylation is a biological process involved in cerebral ischemia. The aim of the present study was to elucidate the effects of S-nitrosylated (SNO) polyethylene glycol-conjugated (PEG) hemoglobin (Hb) developed as an artificial oxygen carrier, which can absorb free NO and translocate NO to a sulfhydryl (SH) moiety, on ischemic cerebral dysfunction. Long-term potentiation (LTP) in the perforant path-dentate gyrus synapses of the rat hippocampus was evaluated as functional outcome 4 days after transient incomplete cerebral ischemia (2-vessel occlusion: 2VO, 10 min). SNO-PEG-Hb (250 mg / kg, i.v.) administered on Day 0, 1, 2, or 4 (immediately, 24 h, 48 h, or 96 h after reperfusion, respectively) alleviated 2VO-induced LTP impairment with a therapeutic time window. The effect was significant when SNO-PEG-Hb was administered on Day 1 or 2. SNO-PEG-Hb altered NOS features observed in the vehicle-treated 2VO rat, upregulation of eNOS, nNOS, and iNOS expressions at mRNA and protein levels; SNO-PEG-Hb further upregulated eNOS and nNOS and downregulated iNOS expressions. These findings suggest that SNO-PEG-Hb might have protective effects on the rat hippocampus from ischemia / reperfusion-induced functional damages, thereby increasing the therapeutic potential as an artificial oxygen carrier for use in the area of oxygen therapy.

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Section: Discussionmentioning

confidence: 88%

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

et al. 2004

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“…We primarily quantified eNOS expression in the penumbra tissue because it is the most important area for rescue after stroke and eNOS expression was most consistently prominent inside the infarct borders in MCAO model. 16) It was showed that the percentages of positive area of eNOS protein immunostaining were consistently increased in the ischemic penumbra compared with the nonischemic side after 2 to 72 h MCAO (Fig. 3), in both of model (Fig.…”

Section: Rqkl Treatment Increases the Immunoactivity Ofmentioning

confidence: 79%

Refined Qing Kai Ling, Traditional Chinese Medicinal Preparation, Reduces Ischemic Stroke-Induced Infarct Size and Neurological Deficits and Increases Expression of Endothelial Nitric Oxide Synthase

Hua

Zhu

et al. 2008

Biological & Pharmaceutical Bulletin

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Refined Qing Kai Ling (RQKL) is an improved injectable multi-component preparation derived from QingKai Ling, which could offer the neuroprotection effect in middle cerebral artery occlusion (MCAO) model of rats by relieving the damage of vascular endothelial cell as well as inhibiting the process of inflammation. Herein, we observed whether RQKL could exert influence on the expression of endothelial nitric oxide synthase (eNOS), as a mechanism of its protective effects against ischemia. Sprague-Dawley rat model of focal cerebral ischemia was established by permanent filament occlusion of the left middle cerebral artery. We found that the administration of RQKL could reduce the ischemic infarct size as well as neurological deficit of model rats. Furthermore, it was showed that the eNOS level was consistently increased in endothelium of blood vessels of the ischemic penumbra after 2 to 72 h of permanent MCAO, and the expression of eNOS increases more in animals treated with RQKL. Our results suggested that eNOS levels in penumbral zone were enhanced after permanent focal ischemia, and RQKL could stimulate postischemic eNOS expression, which may be an important mechanism in RQKL's protection against cerebral ischemia.

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“…The stroke model was prepared in a spontaneously hypertensive rat strain (SHR) as previously described (Leker et al, 2001). Experimental animals were sacrificed 0.5, 1, 2, 12, 24, 48 and 72 h after the operation (two animals per time point).…”

Section: Permanent Middle Cerebral Artery Occlusion (Mcao) Stroke Modelmentioning

confidence: 99%

Identification of a novel stress-responsive gene Hi95 involved in regulation of cell viability

et al. 2002

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cDNA microarray hybridization was used in an attempt to identify novel genes participating in cellular responses to prolonged hypoxia. One of the identified novel genes, designated Hi95 shared significant homology to a p53-regulated GADD family member PA26. In addition to its induction in response to prolonged hypoxia, the increased Hi95 transcription was observed following DNA damage or oxidative stress, but not following hyperthermia or serum starvation. Whereas induction of Hi95 by prolonged hypoxia or by oxidative stress is most likely p53-independent, its induction in response to DNA damaging treatments (g-or UV-irradiation, or doxorubicin) occurs in a p53-dependent manner. Overexpression of Hi95 fulllength cDNA was found toxic for many types of cultured cells directly leading either to their apoptotic death or to sensitization to serum starvation and DNA damaging treatments. Unexpectedly, conditional overexpression of the Hi95 cDNA in MCF7-tet-off cells resulted in their protection against cell death induced by hypoxia/glucose deprivation or H 2 O 2 . Thus, Hi95 gene seems to be involved in complex regulation of cell viability in response to different stress conditions.

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Expression of endothelial nitric oxide synthase in the ischemic penumbra: relationship to expression of neuronal nitric oxide synthase and vascular endothelial growth factor

Cited by 54 publications

References 37 publications

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

An S-Nitrosylated Hemoglobin Derivative Protects the Rat Hippocampus From Ischemia-Induced Long-Term Potentiation Impairment With a Time Window

Refined Qing Kai Ling, Traditional Chinese Medicinal Preparation, Reduces Ischemic Stroke-Induced Infarct Size and Neurological Deficits and Increases Expression of Endothelial Nitric Oxide Synthase

Identification of a novel stress-responsive gene Hi95 involved in regulation of cell viability

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