AP-1 inhibitory peptides attenuate in vitro cortical neuronal cell death induced by kainic acid

@article{Meade2010AP1IP,
  title={AP-1 inhibitory peptides attenuate in vitro cortical neuronal cell death induced by kainic acid},
  author={Amanda J. Meade and Bruno P Meloni and Frank L Mastaglia and Paul M. Watt and Neville W. Knuckey},
  journal={Brain Research},
  year={2010},
  volume={1360},
  pages={8-16}
}
This study has assessed the neuroprotective efficacy of five AP-1 inhibitory peptides in an in vitro excitotoxicity model. The five AP-1 inhibitory peptides and controls of the JNK inhibitor peptide (JNKI-1D-TAT) and TAT cell-penetrating-peptide were administered to primary cortical neuronal cultures prior to kainic acid exposure. All five AP-1 inhibitory peptides and JNKI-1D-TAT provided significant neuroprotection from kainic acid induced neuronal cell death. Kainic acid exposure induced… 
Attenuation of Neuronal Death by Peptide Inhibitors of AP-1 Activation in Acute and Delayed In Vitro Ischaemia (Oxygen/Glucose Deprivation) Models
TLDR
The neuroprotective efficacy of five peptides previously demonstrated to down-regulate AP-1 activation and inhibit neuronal death in vitro following glutamate and kainic acid excitotoxicity is evaluated using acute and delayed in vitro ischaemia models.
Lack of Neuroprotection of Inhibitory Peptides Targeting Jun/JNK after Transient Focal Cerebral Ischemia in Spontaneously Hypertensive Rats
  • William R Gow, Kym Campbell, +4 authors B. Meloni
  • Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2011
TLDR
No treatment significantly reduced infarct volume or improved functional score measurements compared with vehicle-treated animals when assessed 48 hours after MCAO, and assessment of the JNKI-1d-TAT peptide also did not improve histological or functional outcomes at 48Hours after occlusion.
Poly-Arginine and Arginine-Rich Peptides are Neuroprotective in Stroke Models
  • B. Meloni, L. M. Brookes, +6 authors N. Knuckey
  • Chemistry, Medicine
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  • 2015
TLDR
It is demonstrated that poly-arginine and arginine-rich cell-penetrating peptides, are highly neuroProtective, have the capacity to reduce glutamic acid-induced neuronal calcium influx and require heparan sulfate preotoglycan-mediated endocytosis to induce a neuroprotective effect.
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Evidence is reviewed that supports the hypothesis that neuroprotection is mediated by carrier peptide endocytosis and there are strong grounds to regard arginine-rich peptides as a new class of neuroprotective molecules for the treatment of a range of neurological disorders.
The Neuroprotective Efficacy of Cell-Penetrating Peptides TAT, Penetratin, Arg-9, and Pep-1 in Glutamic Acid, Kainic Acid, and In Vitro Ischemia Injury Models Using Primary Cortical Neuronal Cultures
TLDR
Assessment of the TAT and three other CPPs for their neuroprotective properties in cortical neuronal cultures following exposure to glutamic acid, kainic acid, or in vitro ischemia demonstrates that different C PPs have the ability to inhibit neurodamaging events/pathways associated with excitotoxic and ischemic injuries.
Peptides targeting the mitogen-activated protein kinase pathway (JNK/Jun) fail to reduce infarct volume after permanent MCAO in Sprague Dawley rats
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No treatment significantly reduced infarct volume or improved functional score measurements compared to vehicle (saline) treated animals when assessed 24 hours post-MCAO.
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Overall, the pro-viable activity of PTD4 was not correlated with the arginine content but rather with the peptide’s ability to adopt a helical structure in the membrane-mimicking environment, which enhances its cell membrane permeability.
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TLDR
The history of CARPs in neuroprotection is reviewed and the intrinsic biological properties that may contribute to their cytoprotective effects and their usefulness as a broad-acting class of neuroprotective drugs are discussed.
c-Jun N-terminal Kinase (JNK) Signaling as a Therapeutic Target for Alzheimer’s Disease
TLDR
This review aims to explain the rationale behind testing therapies based on inhibition of JNK signaling for AD in terms of current knowledge about the pathophysiology of the disease.
Mitochondria and neuroprotection in stroke: Cationic arginine-rich peptides (CARPs) as a novel class of mitochondria-targeted neuroprotective therapeutics
TLDR
An overview on neuronal mitochondrial dysfunction in ischaemic stroke pathophysiology is provided and the potential beneficial effects of cationic arginine-rich peptides on mitochondria in the ischaemia brain following stroke is highlighted.
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