Identification of proteins regulated by estradiol in focal cerebral ischemic injury—A proteomics approach

Sung, Jin-Hee; Cho, Eun Hae; Min, Wongi; Kim, Mi-Jeong; Kim, Myeong-Ok; Jung, Eun-Jung; Koh, Phil-Ok

doi:10.1016/j.neulet.2010.04.028

Cited by 22 publications

(17 citation statements)

References 36 publications

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“…The proteomics study was performed using a previously described method [15]. Twenty-four hours after MCAO, the right cerebral cortices were isolated, homogenized in lysis buffer (8 M urea, 4% CHAPS, ampholytes, and 40 mM Tris-HCl), and centrifuged at 16,000 g for 20 min at 4℃.…”

Section: Methodsmentioning

confidence: 99%

“…Immobilized pH gradient (IPG) gel strips (17 cm, pH 4-7 and pH 6-9; Bio-Rad) were rehydrated in buffer (8 M urea, 2% CHAPS, 20 mM DTT, 0.5% IPG buffer, and bromophenol blue) for 13 hours. The protein samples (100 µg) were loaded onto the IPG strips using a sample cup and IEF was performed as previously described [15]. The strips were subjected to gradient gels (7.5-17.5%) for sodium dodecyl sulfate (SDS) gel electrophoresis.…”

Section: Methodsmentioning

confidence: 99%

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Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Jang

Koh

2016

Lab Anim Res

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Dynamin-like protein I (DLP-1) is an important mitochondrial fission and fusion protein that is associated with apoptotic cell death in neurodegenerative diseases. In this study, we investigated DLP-1 expression in a focal cerebral ischemia animal model and glutamate-exposed hippocampal-derived cell line. Middle cerebral artery occlusion (MCAO) was surgically induced in adult male rats to induce focal cerebral ischemic injury. Brain tissues were collected 24 hours after the onset of MCAO. MCAO induces an increase in infarct volume and histopathological changes in the cerebral cortex. We identified a decrease in DLP-1 in the cerebral cortices of MCAO-injured animals using a proteomic approach and Western blot analysis. Moreover, glutamate treatment significantly decreased DLP-1 expression in a hippocampal-derived cell line. The decrease in DLP-1 indicates mitochondrial dysfunction. Thus, these results suggest that neuronal cell injury induces a decrease in DLP-1 levels and consequently leads to neuronal cell death.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Jang

Koh

2016

Lab Anim Res

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“…Proteins can be identified en masse by proteomic methods and individual proteins can be quantified by immunoblot or enzyme-linked immunosorbent assays [126,127]. Specific mRNAs are detected and quantified by polymerase chain reaction (PCR)-based gene array methods and by real-time PCR (see [128] for review).…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology, treatment, and animal and cellular models of human ischemic stroke

Woodruff

Thundyil

Tang

et al. 2011

Mol Neurodegeneration

492

367

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Stroke is the world's second leading cause of mortality, with a high incidence of severe morbidity in surviving victims. There are currently relatively few treatment options available to minimize tissue death following a stroke. As such, there is a pressing need to explore, at a molecular, cellular, tissue, and whole body level, the mechanisms leading to damage and death of CNS tissue following an ischemic brain event. This review explores the etiology and pathogenesis of ischemic stroke, and provides a general model of such. The pathophysiology of cerebral ischemic injury is explained, and experimental animal models of global and focal ischemic stroke, and in vitro cellular stroke models, are described in detail along with experimental strategies to analyze the injuries. In particular, the technical aspects of these stroke models are assessed and critically evaluated, along with detailed descriptions of the current best-practice murine models of ischemic stroke. Finally, we review preclinical studies using different strategies in experimental models, followed by an evaluation of results of recent, and failed attempts of neuroprotection in human clinical trials. We also explore new and emerging approaches for the prevention and treatment of stroke. In this regard, we note that single-target drug therapies for stroke therapy, have thus far universally failed in clinical trials. The need to investigate new targets for stroke treatments, which have pleiotropic therapeutic effects in the brain, is explored as an alternate strategy, and some such possible targets are elaborated. Developing therapeutic treatments for ischemic stroke is an intrinsically difficult endeavour. The heterogeneity of the causes, the anatomical complexity of the brain, and the practicalities of the victim receiving both timely and effective treatment, conspire against developing effective drug therapies. This should in no way be a disincentive to research, but instead, a clarion call to intensify efforts to ameliorate suffering and death from this common health catastrophe. This review aims to summarize both the present experimental and clinical state-of-the art, and to guide future research directions.

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“…PEA15 is a multi-functional protein that has been implicated in the regulation of major intracellular processes including proliferation and apoptosis, and its function is tightly regulated by its phosphorylation at two serine residues, Ser104 and Ser116 [27]. Both CaMKII and AKT phosphorylate PEA15 at Ser116 [47][48][49] and, more recently, AMPK was reported to act as an upstream kinase of PEA15 in both normal and cancerous breast epithelial cells [36]. Phosphatases play an equally important role as kinases in regulating the phosphorylation state of PEA15.…”

Section: Discussionmentioning

confidence: 99%

The protein phosphatase 4 - PEA15 axis regulates the survival of breast cancer cells

Mohammed

Pickard

Mourtada-Maarabouni

2016

Cellular Signalling

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Identification of proteins regulated by estradiol in focal cerebral ischemic injury—A proteomics approach

Cited by 22 publications

References 36 publications

Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Ischemic brain injury decreases dynamin-like protein 1 expression in a middle cerebral artery occlusion animal model and glutamate-exposed HT22 cells

Pathophysiology, treatment, and animal and cellular models of human ischemic stroke

The protein phosphatase 4 - PEA15 axis regulates the survival of breast cancer cells

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