New Avenues of Exploration for Erythropoietin

Maiese, Kenneth; Li, Faqi; Chong, Zhao Zhong

doi:10.1001/jama.293.1.90

Cited by 495 publications

(528 citation statements)

References 47 publications

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“…Cellular membrane PS exposure can precipitate the subsequent removal of cells in the nervous system by activated microglia [26][27][28]. We illustrate that exposure to Aβ results in the significant externalization of PS that can be blocked by Wnt1 overexpression.…”

Section: Discussionmentioning

confidence: 97%

“…Subsequent externalization of membrane PS residues in neurons undergoing apoptosis can result in inflammatory cell activation and identify these cells for phagocytic disposal [26][27][28]. We therefore examined the ability of Wnt1 to modulate externalization of membrane PS exposure in SH-SY5Y cells during Aβ 1-42 exposure.…”

Section: Wnt1 Blocks Apoptotic Membrane Phosphatidylserine (Ps) Exposmentioning

confidence: 99%

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Cellular demise and inflammatory microglial activation during β-amyloid toxicity are governed by Wnt1 and canonical signaling pathways

Chong

Maiese

2007

Cellular Signalling

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164

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Initially described as a modulator of embryogenesis for a number of organ systems, Wnt1 has recently been linked to the development of several neurodegenerative disorders, none being of greater significance than Alzheimer's disease. We therefore examined the ability of Wnt1 to oversee vital pathways responsible for cell survival during β-amyloid (Aβ 1-42 )exposure. Here we show that Wnt1 is critical for protection in the SH-SY5Y neuronal cell line against genomic DNA degradation, membrane phosphatidylserine (PS) exposure, and microglial activation, since these neuroprotective attributes of Wnt1 are lost during gene silencing of Wnt1 protein expression. Intimately tied to Wnt1 protection is the presence and activation of Akt1. Pharmacological inhibition of the PI 3-K pathway or gene silencing of Akt1 expression can abrogate the protective capacity of Wnt1. Closely aligned with Wnt1 and Akt1 are the integrated canonical pathways of synthase kinase-3β (GSK-3β) and β-catenin. Through Akt1 dependent pathways, Wnt1 phosphorylates GSK-3β and maintains β-catenin integrity to insure its translocation from the cytoplasm to the nucleus to block apoptosis. Our work outlines a highly novel role for Wnt1 and its integration with Akt1, GSK-3β, and β-catenin to foster neuronal cell survival and repress inflammatory microglial activation that can identify new avenues of therapy against neurodegenerative disorders.

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Section: Discussionmentioning

confidence: 97%

Section: Wnt1 Blocks Apoptotic Membrane Phosphatidylserine (Ps) Exposmentioning

confidence: 99%

Cellular demise and inflammatory microglial activation during β-amyloid toxicity are governed by Wnt1 and canonical signaling pathways

Chong

Maiese

2007

Cellular Signalling

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164

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“…In neurons, Bcl-xL is shown to be strongly expressed after EPO is administrated [36] . In addition, more recent work in cerebral microvascular endothelial cells (ECs) illustrates that upregulation of Bcl-xL by EPO may be necessary for preventing apoptosis [37,38] . Our present study showed that MPP + significantly increased the ratio of the pro-apoptotic Bax to the anti-apoptotic Bcl-2, which consists with the previous studies [22,39] .…”

Section: Discussionmentioning

confidence: 99%

Protective effect of erythropoietin against 1-methyl-4-phenylpyridinium-induced neurodegenaration in PC12 cells

Shang

Sun

et al. 2007

Neurosci. Bull.

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Objective The neuroprotective effect of erythropoietin (EPO) against 1-methyl-4-phenylpyridinium (MPP + )-induced oxidative stress in cultured PC12 cells, as well as the underlying mechanism, were investigated. Methods PC12 cells impaired by MPP + were used as the cell model of Parkinson's disease. Methyl thiazolyl tetrazolium (MTT) was used to assay the viability of the PC12 cells exposed to gradient concentrations of EPO, and the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay was used to analyze the apoptosis ratio of PC12 cells. The expression of Bcl-2 and Bax in PC12 cells were examined by Western blot, and the reactive oxygen species (ROS), the mitochondrial transmembrane potential and the activity of caspase-3 in each group were detected by spectrofluorometer. Results Treatment of PC12 cells with MPP + caused the loss of cell viability, which may be associated with the elevation in apoptotic rate, the formation of ROS and the disruption of mitochondrial transmembrane potential. It was also shown that MPP + significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3. In contrast, EPO significantly reversed these responses and had the maximum protective effect at 1 U/mL. Conclusion The inhibitive effect of EPO on the MPP + -induced cytotoxicity may be ascribed to its anti-oxidative property and anti-apoptotic activity, and EPO may provide a useful therapeutic strategy for treatment of neurodegenerative diseases such as Parkinson's disease.

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“…In addition to the kidney and liver, EPO mRNA has been detected in other tissues including myocardium, brain and bone marrow. The EPO receptor (EPOR) is also found in cardiomyocytes and endothelial cells (Maiese et al, 2005). EPO plays important roles in erythropoiesis, as well as in cardiogenesis (Stuckmann et al, 2003).…”

Section: Erythropoietin/erythropoietin Receptormentioning

confidence: 99%

Migration of Resident Cardiac Stem Cells in Myocardial Infarction

Liang

Phillips

2012

The Anatomical Record

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Ischemic heart disease is a major cause of morbidity and mortality worldwide. Stem cell-based therapy, which aims to restore cardiac structure and function by regeneration of functional myocardium, has recently been proposed as a novel alternative treatment modality. Resident cardiac stem cells (CSCs) in adult hearts are a key cell type under investigation. CSCs have been shown to be able to repair damaged myocardium and improve myocardial function in both human and animal studies. This approach relies not only on the proliferation of the CSCs, but also upon their migration to the site of injury within the heart. Here, we briefly review reported CSC populations and discuss signaling factors and pathways required for the migration of CSCs. Anat Rec, 296:184-191, 2013. V C 2012 Wiley Periodicals, Inc.

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New Avenues of Exploration for Erythropoietin

Cited by 495 publications

References 47 publications

Cellular demise and inflammatory microglial activation during β-amyloid toxicity are governed by Wnt1 and canonical signaling pathways

Cellular demise and inflammatory microglial activation during β-amyloid toxicity are governed by Wnt1 and canonical signaling pathways

Protective effect of erythropoietin against 1-methyl-4-phenylpyridinium-induced neurodegenaration in PC12 cells

Migration of Resident Cardiac Stem Cells in Myocardial Infarction

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