Effect of erythropoietin on staurosporine-induced apoptosis and differentiation of SH-SY5Y neuroblastoma cells

Pregi, Nicolás; Vittori, Daniela; Pérez, Gladys; Leirós, Claudia Pérez; Nesse, Alcira

doi:10.1016/j.bbamcr.2005.12.011

Cited by 40 publications

(49 citation statements)

References 40 publications

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“…In cells that involve the brain or the retina, EPO can prevent injury from hypoxic ischemia (Chong et al, 2002b;Liu et al, 2006;Meloni et al, 2006;Wei et al, 2006;Yu et al, 2005), excitotoxicity (Montero et al, 2007;Yamasaki et al, 2005), infection (Kaiser et al, 2006), free radical exposure Chong et al, 2003e;Yamasaki et al, 2005), staurosporine (Pregi et al, 2006), and dopaminergic cell injury (Demers et al, 2005;McLeod et al, 2006;Signore et al, 2006). In addition, administration of EPO also represents a viable option for the prevention of retinal cell injury during glutamate toxicity (Zhong et al, 2007) and glaucoma (Tsai et al, 2007).…”

Section: Epo and Neurodegenerationmentioning

confidence: 99%

Erythropoietin: Elucidating new cellular targets that broaden therapeutic strategies

Maiese

Chong

et al. 2008

Progress in Neurobiology

102

155

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Given that erythropoietin (EPO) is no longer believed to have exclusive biological activity in the hematopoietic system, EPO is now considered to have applicability in a variety of nervous system disorders that can overlap with vascular disease, metabolic impairments, and immune system function. As a result, EPO may offer efficacy for a broad number of disorders that involve Alzheimer's disease, cardiac insufficiency, stroke, trauma, and diabetic complications. During a number of clinical conditions, EPO is robust and can prevent metabolic compromise, neuronal and vascular degeneration, and inflammatory cell activation. Yet, use of EPO is not without its considerations especially in light of frequent concerns that may compromise clinical care. Recent work has elucidated a number of novel cellular pathways governed by EPO that can open new avenues to avert deleterious effects of this agent and offer previously unrecognized perspectives for therapeutic strategies. Obtaining greater insight into the role of EPO in the nervous system and elucidating its unique cellular pathways may provide greater cellular viability not only in the nervous system but also throughout the body.

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Section: Epo and Neurodegenerationmentioning

confidence: 99%

Erythropoietin: Elucidating new cellular targets that broaden therapeutic strategies

Maiese

Chong

et al. 2008

Progress in Neurobiology

102

155

View full text Add to dashboard Cite

show abstract

“…In cells that involve the brain or the retina, EPO can prevent injury from hypoxic ischemia , Chong, et al, 2002b, Liu, et al, 2006, Meloni, et al, 2006, Wei, et al, 2006, Yu, et al, 2005, excitotoxicity (Montero, et al, 2007, Yamasaki, et al, 2005, infection (Kaiser, et al, 2006), free radical exposure , Chong, et al., 2003e, Yamasaki, et al, 2005, staurosporine (Pregi, et al, 2006), and dopaminergic cell injury (Demers, et al, 2005, McLeod, et al, 2006. In addition, administration of EPO also represents a viable option for the prevention of retinal cell injury during glaucoma (Tsai, et al, 2007).…”

Section: Immune Function and The Nervous Systemmentioning

confidence: 99%

Erythropoietin and Oxidative Stress

Maiese

Chong

Hou

et al. 2008

CNR

108

113

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Unmitigated oxidative stress can lead to diminished cellular longevity, accelerated aging, and accumulated toxic effects for an organism. Current investigations further suggest the significant disadvantages that can occur with cellular oxidative stress that can lead to clinical disability in a number of disorders, such as myocardial infarction, dementia, stroke, and diabetes. New therapeutic strategies are therefore sought that can be directed toward ameliorating the toxic effects of oxidative stress. Here we discuss the exciting potential of the growth factor and cytokine erythropoietin for the treatment of diseases such as cardiac ischemia, vascular injury, neurodegeneration, and diabetes through the modulation of cellular oxidative stress. Erythropoietin controls a variety of signal transduction pathways during oxidative stress that can involve Janus-tyrosine kinase 2, protein kinase B, signal transducer and activator of transcription pathways, Wnt proteins, mammalian forkhead transcription factors, caspases, and nuclear factor κB. Yet, the biological effects of erythropoietin may not always be beneficial and may be poor tolerated in a number of clinical scenarios, necessitating further basic and clinical investigations that emphasize the elucidation of the signal transduction pathways controlled by erythropoietin to direct both successful and safe clinical care. KeywordsAlzheimer's disease; Akt; angiogenesis; apoptosis; cancer; cardiac; caspases; diabetes; endothelial; erythropoietin; forkhead; FoxO; GSK-3β; inflammation; mitochondria; NF-κB; renal; STATs; Wnt OXIDATIVE STRESSInitial work in pathways that can lead to oxidative stress by early investigators observed that increased metabolic rates could be detrimental to animals in an elevated oxygen environment. More current studies point to the potential aging mechanisms and accumulated toxic effects for an organism that are tied to oxidative stress (Maiese, et al., 2008a NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript in organisms, or at least the rate of oxygen consumption in organisms, has intrigued several investigators. Pearl proposed that increased exposure to oxygen through an increased metabolic rate could lead to a shortened life span (Pearl, 1928). Subsequent work by multiple investigators has furthered this hypothesis by demonstrating that increased metabolic rates could be detrimental to animals in an elevated oxygen environment . When one moves to more current work, oxygen free radicals and mitochondrial DNA mutations have become associated with oxidative stress injury, aging mechanisms, and accumulated toxicity for an organism (Yui and Matsuura, 2006).Oxygen free radicals can be generated in elevated quantities during the reduction of oxygen and subsequently lead to cell injury and apoptosis. Oxidative stress occurs as a result of the development of reactive oxygen species that consist of oxygen free radicals and other chemical entities. These agents can involve superoxide free radicals, hydrogen peroxide, sin...

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“…Acinar cells were collected in culture medium, pelleted and homogenized as previously reported [18] . Digestion was allowed to proceed, proteinase K was added and then, after precipitation electrophoresis was carried out on 2% agarose gel, bands were observed under UV transilluminator and digitalized [18] .…”

Section: Detection Of Dna Fragmentationmentioning

confidence: 99%

“…Digestion was allowed to proceed, proteinase K was added and then, after precipitation electrophoresis was carried out on 2% agarose gel, bands were observed under UV transilluminator and digitalized [18] .…”

Section: Detection Of Dna Fragmentationmentioning

confidence: 99%

NOD Mice Exocrinopathy: Towards a Neuroimmune Link

Calafat

Larocca²,

Roca³

et al. 2007

Neuroimmunomodulation

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Sjögren’s syndrome (SS) is a chronic autoimmune disorder of exocrine glands characterized as an autoimmune exocrinopathy and more specifically as an autoimmune epithelitis. An impaired balance of neuroimmune interactions mediated by vasoactive intestinal peptide (VIP) in the target organ at early stages of disease is explored by means of the nonobese diabetic (NOD) mouse model of SS. We have previously described a reduced salivary secretion and signaling upon VIP stimulation. The effect reflected a differential regulation of the neural isoform of nitric oxide synthase by calcium calmodulin kinase II and occurred prior to the appearance of detectable levels of cytokines in NOD glands. VIP acting on NOD macrophages treated with lipopolysaccharide promoted anti-inflammatory effects by inhibiting nitric oxide synthase induction as well as IL-12 and TNF-α production, while stimulating IL-10. Here we present evidence on the ability of apoptotic acinar cells from submandibular glands of NOD mice to stimulate nitric oxide in both peritoneal and glandular macrophage pools to a similar extent as lipopolysaccharide + IFN-γ. VIP was not effective to prevent nitrite accumulation and modestly increased IL-10 levels in macrophages coincubated with acinar cells. An enhanced nitrite response of NOD glandular macrophages in basal and stimulated conditions compared to peritoneal cells is also shown.

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Effect of erythropoietin on staurosporine-induced apoptosis and differentiation of SH-SY5Y neuroblastoma cells

Cited by 40 publications

References 40 publications

Erythropoietin: Elucidating new cellular targets that broaden therapeutic strategies

Erythropoietin: Elucidating new cellular targets that broaden therapeutic strategies

Erythropoietin and Oxidative Stress

NOD Mice Exocrinopathy: Towards a Neuroimmune Link

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