Protective effect of colostrinin on neuroblastoma cell survival is due to reduced aggregation of β-amyloid

Schuster, David; Rajendran, Anitha; Hui, Sek Wen; Nicotera, Thomas M.; Srikrishnan, T.; Kruzel, Marian L.

doi:10.1016/j.npep.2005.03.005

Cited by 36 publications

(36 citation statements)

References 20 publications

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“…We examined dose-dependent effects of minocycline over Ab 1-42 treatment (30 mM, 24 h). The condition of Ab 1-42 treatment at 30 mM for 24 h was chosen based on our preliminary study (data not shown) and study by others (Schuster et al, 2005), in which 25 mM concentration of Ab 1-42 reduced cell viability by about 20%. Minocycline at concentrations of 1, 5, 10, 20 mM minocycline were pretreated in differentiated PC 12 cells 24 h before Ab 1-42 treatment.…”

Section: Minocycline Inhibited the Increases In P-eif2a And Reduced Tmentioning

confidence: 99%

Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models

Choi

Kim

Shin

et al. 2007

Neuropsychopharmacol

259

179

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Minocycline is a semi-synthetic tetracycline antibiotic that effectively crosses the blood-brain barrier. Minocycline has been reported to have significant neuroprotective effects in models of cerebral ischemia, traumatic brain injury, amyotrophic lateral sclerosis, and Huntington's and Parkinson's diseases. In this study, we demonstrate that minocycline has neuroprotective effects in in vitro and in vivo Alzheimer's disease models. Minocycline was found to attenuate the increases in the phosphorylation of double-stranded RNAdependent serine/threonine protein kinase, eukaryotic translation initiation factor-2 a and caspase 12 activation induced by amyloid b peptide 1-42 treatment in NGF-differentiated PC 12 cells. In addition, increases in the phosphorylation of eukaryotic translation initiation factor-2 a were attenuated by administration of minocycline in Tg2576 mice, which harbor mutated human APP695 gene including the Swedish double mutation and amyloid b peptide 1-42 -infused rats. We found that minocycline administration attenuated deficits in learning and memory in amyloid b peptide 1-42 -infused rats. Increased phosphorylated state of eukaryotic translation initiation factor-2 a is observed in Alzheimer's disease patients' brains and may result in impairment of cognitive functions in Alzheimer's disease patients by decreasing the efficacy of de novo protein synthesis required for synaptic plasticity. On the basis of these results, minocycline may prove to be a good candidate as an effective therapeutic agent for Alzheimer's disease.

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Section: Minocycline Inhibited the Increases In P-eif2a And Reduced Tmentioning

confidence: 99%

Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models

Choi

Kim

Shin

et al. 2007

Neuropsychopharmacol

259

179

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“…Most importantly, CLN induces delicate cassettes of signaling pathways common to cell proliferation and differentiation and mediates cellular activities that are similar to those of hormones and neurotrophins, leading to neurite outgrowth [9]. CLN protects neuroblastoma cells from β-amyloid-induced apoptosis by inhibiting amyloid aggregation [10]. CLN delays the onset of proliferative senescence of diploid murine fibroblast cells [11].…”

Section: Introductionmentioning

confidence: 99%

Colostrinin Decreases Hypersensitivity and Allergic Responses to Common Allergens

Boldogh¹,

Aguilera-Aguirre²,

Bácsi³

et al. 2008

Int Arch Allergy Immunol

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Background: Colostrinin™ (CLN), isolated from mothers’ pre-milk fluid (colostrum), is a uniform mixture of low-molecular-weight, proline-rich polypeptides. CLN induces neurite outgrowth of pheochromocytoma cells, extends the lifespan of diploid fibroblast cells, inhibits β-amyloid-induced apoptosis and improves cognitive functions when administered to Alzheimer’s disease patients. Objective: The aim of this study was to investigate potential allergic responses to CLN and its impact on allergic sensitization and inflammation caused by common allergens. Methods: We used a well-characterized mouse model of allergic airway inflammation. Changes in IgE/IgG1 and mucin levels, airway eosinophilia and hyperreactivity to methacholine were determined by ELISA, differential cell counting and whole-body plethysmography, respectively. Results: CLN did not increase IgE/IgG1 levels or induce cutaneous hypersensitivity reaction, airway inflammation and mucin production. Importantly, CLN significantly (p < 0.001) decreased IgE/IgG1 production, airway eosinophilia, mucin production and hypersensitivity induced by allergenic extracts from ragweed pollen grains and house dust mites. Conclusion: CLN itself is non-allergenic; however, it is effective in preventing allergic responses to known indoor and outdoor allergens. These data support the safe application of CLN and its potential use in the prevention of allergic inflammation in humans.

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“…The RevertAid TM First Strand cDNA Synthesis Kit was from Fermentas (Life Sciences). 1H- [1,2,4] oxadiazolo [4,3-a]quinoxalin-1-one (ODQ) and 1-methyl-3-isobutylxanthine (IBMX) were from Cayman Chemical (San Diego, CA). Monoclonal antibody: anti-nNOS, anti-ERK1/2, and anti-phospho-ERK1/ 2, and U0126-selective MEK 1/2 inhibitor were from Cell Signaling (Boston, MA).…”

Section: Methodsmentioning

confidence: 99%

“…Another possibility to explain the therapeutic effect of PRP/Colostrinin is its effect on neurite outgrowth. Also, Colostrinin, as well as its constituent nonapeptide not only inhibits aggregation of amyloid b and formation of fibrillar structures but also can dissolve aggregates already formed, acting as a b-sheet breaker [1,2]. Nerve growth factor (NGF) is a neurotrophin that has been shown to exert a number of different, distinguishable effects on neurons, such as survival, growth of fibers, and differentiation of target neurons [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

et al. 2014

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Naturally occurring compounds that can act as prosurvival factors and neurite formation stimulants in the conditions of reduced neurotrophins production are important both in neuronal protection and therapy of neurodegenerative disorders. Therefore, the role of proline-rich polypeptide complex (PRP) and its nonapeptide fragment (NP) in the promotion of pheochromocytoma cell line (PC12) survival and neurite outgrowth pathway is presented. It was shown that PRP/NP did not affect the neuronal nitric oxide synthase (nNOS) at the transcriptional and protein level. However, the activity of nNOS and intracellular nitric oxide (NO) concentration was markedly increased after treatment of PC12 cells with peptides. This reaction was inhibited by L-NAME-nNOS inhibitor. It was shown that PRP and NP induce the soluble guanylyl cyclase to release higher amount of cyclic GMP (cGMP), and subsequently, the increased phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) is observed. This effect was abolished by both U0126 (inhibitor of ERK1/2) and also by L-NAME. Reduction of ERK1/2 activity observed in the presence of nNOS inhibitor suggests that its activation is NO-dependent. The presented results shed some light on the mechanism of action of PRP complex. PRP and NP can activate NO/cGMP/ERK1/2 signaling pathway, similarly to nerve growth factor (NGF). The prosurvival action and short fibers formation suggest the role of PRP and NP in neuroprotection and the initiation of neuritogenesis. They can also participate in the amplification of signals controlling the survival and differentiation of neurons effect when the deficit of NGF takes place.

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Protective effect of colostrinin on neuroblastoma cell survival is due to reduced aggregation of β-amyloid

Cited by 36 publications

References 20 publications

Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models

Minocycline Attenuates Neuronal Cell Death and Improves Cognitive Impairment in Alzheimer's Disease Models

Colostrinin Decreases Hypersensitivity and Allergic Responses to Common Allergens

Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

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