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Article: Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke.

Meloni, Bruno P

2017 Volume 7, Issue 8

Abstract: Hypoxic-ischemic brain injury and stroke are closely related and devastating conditions that can affect individuals of all ages.[ ... ]. ...

Abstract	Hypoxic-ischemic brain injury and stroke are closely related and devastating conditions that can affect individuals of all ages.[...].
Language	English
Publishing date	2017-08-22
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci7080110
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Article: The Poly-Arginine Peptide R18D Interferes with the Internalisation of α-Synuclein Pre-Formed Fibrils in STC-1 Enteroendocrine Cells.

Gorecki, Anastazja M / Spencer, Holly / Meloni, Bruno P / Anderton, Ryan S

Biomedicines

2023 Volume 11, Issue 8

Abstract: In Parkinson's disease (PD), gut inflammation is hypothesised to contribute to α-synuclein aggregation, but gastrointestinal α-synuclein expression is poorly characterised. Cationic arginine-rich peptides (CARPs) are an emerging therapeutic option that ... ...

Abstract	In Parkinson's disease (PD), gut inflammation is hypothesised to contribute to α-synuclein aggregation, but gastrointestinal α-synuclein expression is poorly characterised. Cationic arginine-rich peptides (CARPs) are an emerging therapeutic option that exerts various neuroprotective effects and may target the transmission of protein aggregates. This study aimed to investigate endogenous α-synuclein expression in enteroendocrine STC-1 cells and the potential of the CARP, R18D (18-mer of D-arginine), to prevent internalisation of pre-formed α-synuclein fibrils (PFFs) in enteroendocrine cells in vitro. Through confocal microscopy, the immunoreactivity of full-length α-synuclein and the serine-129 phosphorylated form (pS129) was investigated in STC-1 (mouse enteroendocrine) cells. Thereafter, STC-1 cells were exposed to PFFs tagged with Alexa-Fluor 488 (PFF-488) for 2 and 24 h and R18D-FITC for 10 min. After confirming the uptake of both PFFs and R18D-FITC through fluorescent microscopy, STC-1 cells were pre-treated with R18D (5 or 10 μM) for 10 min prior to 2 h of PFF-488 exposure. Immunoreactivity for endogenous α-synuclein and pS129 was evident in STC-1 cells, with prominent pS129 staining along cytoplasmic processes and in perinuclear areas. STC-1 cells internalised PFFs, confirmed through co-localisation of PFF-488 and human-specific α-synuclein immunoreactivity. R18D-FITC entered STC-1 cells within 10 min and pre-treatment of STC-1 cells with R18D interfered with PFF uptake. The endogenous presence of α-synuclein in enteroendocrine cells, coupled with their rapid uptake of PFFs, demonstrates a potential for pathogenic spread of α-synuclein aggregates in the gut. R18D is a novel therapeutic approach to reduce the intercellular transmission of α-synuclein pathology.
Language	English
Publishing date	2023-07-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11082089
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Article: Arginine and Arginine-Rich Peptides as Modulators of Protein Aggregation and Cytotoxicity Associated With Alzheimer's Disease.

Mamsa, Somayra S A / Meloni, Bruno P

Frontiers in molecular neuroscience

2021 Volume 14, Page(s) 759729

Abstract: A substantial body of evidence indicates cationic, arginine-rich peptides (CARPs) are effective therapeutic compounds for a range of neurodegenerative pathologies, with beneficial effects including the reduction of excitotoxic cell death and ... ...

Abstract	A substantial body of evidence indicates cationic, arginine-rich peptides (CARPs) are effective therapeutic compounds for a range of neurodegenerative pathologies, with beneficial effects including the reduction of excitotoxic cell death and mitochondrial dysfunction. CARPs, therefore, represent an emergent class of promising neurotherapeutics with multimodal mechanisms of action. Arginine itself is a known chaotrope, able to prevent misfolding and aggregation of proteins. The putative role of proteopathies in chronic neurodegenerative diseases such as Alzheimer's disease (AD) warrants investigation into whether CARPs could also prevent the aggregation and cytotoxicity of amyloidogenic proteins, particularly amyloid-beta and tau. While monomeric arginine is well-established as an inhibitor of protein aggregation in solution, no studies have comprehensively discussed the anti-aggregatory properties of arginine and CARPs on proteins associated with neurodegenerative disease. Here, we review the structural, physicochemical, and self-associative properties of arginine and the guanidinium moiety, to explore the mechanisms underlying the modulation of protein aggregation by monomeric and multimeric arginine molecules. Arginine-rich peptide-based inhibitors of amyloid-beta and tau aggregation are discussed, as well as further modulatory roles which could reduce proteopathic cytotoxicity, in the context of therapeutic development for AD.
Language	English
Publishing date	2021-10-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2021.759729
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Article ; Online: Impact of poly-arginine peptides R18D and R18 on alteplase and tenecteplase thrombolysis in vitro, and neuroprotective stability to proteolysis.

Meloni, Bruno P / Blacker, David J / Edwards, Adam B / Knuckey, Neville W

Journal of thrombosis and thrombolysis

2022 Volume 54, Issue 1, Page(s) 172–182

Abstract: The poly-arginine peptides R18D and R18 represent novel potential neuroprotective treatments for acute ischaemic stroke. Here we examined whether R18D and R18 had any significant effects on the thrombolytic activity of alteplase (tPA) and tenecteplase ( ... ...

Abstract	The poly-arginine peptides R18D and R18 represent novel potential neuroprotective treatments for acute ischaemic stroke. Here we examined whether R18D and R18 had any significant effects on the thrombolytic activity of alteplase (tPA) and tenecteplase (TNK) on clots formed from whole blood in an in vitro thrombolysis plate assay. R18D and R18 were examined at concentrations of 0.25, 0.5, 1, 2, 4, 8 and 16 µM during the 1-h thrombolytic assay. We also included the well-characterised neuroprotective NA-1 peptide as a control. R18D, R18 and NA-1 all reduced tPA or TNK percentage clot lysis by 0-9.35%, 0-3.44% and 0-4.8%, respectively. R18D, R18 and NA-1 had a modest and variable effect on the lag time, increasing the time to the commencement of thrombolysis by 0-9.9 min, 0-5.53 min and 0-7.16 min, respectively. Lastly, R18 and NA-1 appeared to increase the maximal activity of the thrombolysis reaction. In addition, the in vitro anti-excitotoxic neuroprotective efficacy of R18D and R18 was not affected by pre-incubation for 1-2 h or overnight with tPA or TNK, whereas only R18D retained high anti-excitotoxic neuroprotective efficacy when pre-incubated in a synthetic trypsin (TrypLE Express). The present in vitro findings suggest that neither R18D or R18 when co-administered with the thrombolytic inducing agents tPA or TNK are likely to have a significant impact when used clinically during clot thrombolysis and confirm the superior proteolytic stability of the R18D peptide.
MeSH term(s)	Arginine ; Brain Ischemia ; Fibrinolytic Agents/pharmacology ; Fibrinolytic Agents/therapeutic use ; Humans ; Peptides/pharmacology ; Proteolysis ; Stroke/drug therapy ; Tenecteplase/pharmacology ; Tenecteplase/therapeutic use ; Thrombolytic Therapy ; Thrombosis ; Tissue Plasminogen Activator/pharmacology ; Tissue Plasminogen Activator/therapeutic use
Chemical Substances	Fibrinolytic Agents ; Peptides ; polyarginine (25212-18-4) ; Arginine (94ZLA3W45F) ; Tissue Plasminogen Activator (EC 3.4.21.68) ; Tenecteplase (WGD229O42W)
Language	English
Publishing date	2022-03-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1230645-9
ISSN	1573-742X ; 0929-5305
ISSN (online)	1573-742X
ISSN	0929-5305
DOI	10.1007/s11239-022-02642-4
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Article: Corrigendum to "Microglia are both a source and target of extracellular cyclophilin A" [Heliyon 5(9) August 2019 e02390].

Flora, Gurkiran Kaur / Anderton, Ryan S / Meloni, Bruno P / Guillemin, Gilles J / Knuckey, Neville W / MacDougall, Gabriella / Matthews, Vance / Boulos, Sherif

Heliyon

2023 Volume 9, Issue 2, Page(s) e12842

Abstract: This corrects the article DOI: 10.1016/j.heliyon.2019.e02390.]. ...

Abstract	[This corrects the article DOI: 10.1016/j.heliyon.2019.e02390.].
Language	English
Publishing date	2023-01-12
Publishing country	England
Document type	Published Erratum
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e12842
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Article ; Online: Emerging cytoprotective peptide therapies for stroke.

Meloni, Bruno P / Blacker, David J / Mastaglia, Frank L / Knuckey, Neville W

Expert review of neurotherapeutics

2020 Volume 20, Issue 9, Page(s) 887–890

Language	English
Publishing date	2020-08-19
Publishing country	England
Document type	Editorial
ZDB-ID	2112534-X
ISSN	1744-8360 ; 1473-7175
ISSN (online)	1744-8360
ISSN	1473-7175
DOI	10.1080/14737175.2020.1788390
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Article: Cationic Arginine-Rich Peptides (CARPs): A Novel Class of Neuroprotective Agents With a Multimodal Mechanism of Action.

Meloni, Bruno P / Mastaglia, Frank L / Knuckey, Neville W

Frontiers in neurology

2020 Volume 11, Page(s) 108

Abstract: There are virtually no clinically available neuroprotective drugs for the treatment of acute and chronic neurological disorders, hence there is an urgent need for the development of new neuroprotective molecules. Cationic arginine-rich peptides (CARPs) ... ...

Abstract	There are virtually no clinically available neuroprotective drugs for the treatment of acute and chronic neurological disorders, hence there is an urgent need for the development of new neuroprotective molecules. Cationic arginine-rich peptides (CARPs) are an expanding and relatively novel class of compounds, which possess intrinsic neuroprotective properties. Intriguingly, CARPs possess a combination of biological properties unprecedented for a neuroprotective agent including the ability to traverse cell membranes and enter the CNS, antagonize calcium influx, target mitochondria, stabilize proteins, inhibit proteolytic enzymes, induce pro-survival signaling, scavenge toxic molecules, and reduce oxidative stress as well as, having a range of anti-inflammatory, analgesic, anti-microbial, and anti-cancer actions. CARPs have also been used as carrier molecules for the delivery of other putative neuroprotective agents across the blood-brain barrier and blood-spinal cord barrier. However, there is increasing evidence that the neuroprotective efficacy of many, if not all these other agents delivered using a cationic arginine-rich cell-penetrating peptide (CCPPs) carrier (e.g., TAT) may actually be mediated largely by the properties of the carrier molecule, with overall efficacy further enhanced according to the amino acid composition of the cargo peptide, in particular its arginine content. Therefore, in reviewing the neuroprotective mechanisms of action of CARPs we also consider studies using CCPPs fused to a putative neuroprotective peptide. We review the history of CARPs in neuroprotection and discuss in detail the intrinsic biological properties that may contribute to their cytoprotective effects and their usefulness as a broad-acting class of neuroprotective drugs.
Language	English
Publishing date	2020-02-25
Publishing country	Switzerland
Document type	Systematic Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2020.00108
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Article: Brain Sciences Special Issue: Neuroprotection against Ischemic Brain Injury.

Meloni, Bruno P

Brain sciences

2013 Volume 3, Issue 3, Page(s) 1415–1416

Abstract: It was my great pleasure to have acted as the guest editor for the Brain Sciences Special Issue on Neuroprotection against Ischemic Brain Injury. This Special Issue consists of a total of 18 articles covering a range of topics with the purpose of ... ...

Abstract	It was my great pleasure to have acted as the guest editor for the Brain Sciences Special Issue on Neuroprotection against Ischemic Brain Injury. This Special Issue consists of a total of 18 articles covering a range of topics with the purpose of providing new knowledge and exploring novel interventions that one day may be used to better protect and repair the brain after ischemia. [...].
Language	English
Publishing date	2013-09-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci3031415
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Article ; Online: Neuroprotective Cationic Arginine-Rich Peptides (CARPs): An Assessment of Their Clinical Safety.

Edwards, Adam B / Mastaglia, Frank L / Knuckey, Neville W / Meloni, Bruno P

Drug safety

2020 Volume 43, Issue 10, Page(s) 957–969

Abstract: Cationic arginine-rich peptides represent a novel class of peptides being developed as neuroprotective agents for stroke and other acute and chronic neurological disorders. As a group, cationic arginine-rich peptides have a diverse range of other ... ...

Abstract	Cationic arginine-rich peptides represent a novel class of peptides being developed as neuroprotective agents for stroke and other acute and chronic neurological disorders. As a group, cationic arginine-rich peptides have a diverse range of other biological properties including the ability to traverse cell membranes, modulate immune responses, antagonise ion channel receptor function, as well as possessing cardioprotective, anti-nociceptive, anti-microbial and anti-cancer properties. A sound understanding of their safety profile is essential for the design of future clinical trials and for ensuring translational success with these compounds. At present, while many neuroprotective cationic arginine-rich peptides have been examined in preclinical animal neuroprotection studies, few have been assessed in human safety studies. Despite this, the safety of the prototypical cationic arginine-rich peptide, protamine, which has been in clinical use for over 70 years to reverse the anticoagulant effects of heparin and as an excipient in certain insulin preparations, is well established. In addition, the poly-arginine peptide R9 (ALX40-4C) was developed as an anti-human inmmunodeficiency virus therapeutic in the mid-1990s, and more recently, the neuroprotective cationic arginine-rich peptides TAT-NR2B9c (NA-1), CN-105 and RD2 are being evaluated for the treatment of ischaemic stroke, haemorrhagic stroke and Alzheimer's disease, respectively. Based on the available clinical data, cationic arginine-rich peptides as a group appear to be safe when administered at therapeutic doses by a slow intravenous infusion. While protamine, owing to its isolation from salmon milt and homology with human sperm protamine, can trigger anaphylactic and anaphylactoid reactions in a small proportion of patients previously exposed to the peptide (e.g. diabetic patients), who are allergic to fish or have undergone a vasectomy, such reactions are unlikely to be triggered in individuals exposed to non-protamine cationic arginine-rich peptides.
MeSH term(s)	Humans ; Neuroprotective Agents/administration & dosage ; Neuroprotective Agents/therapeutic use ; Peptides/administration & dosage ; Peptides/therapeutic use ; Stroke/prevention & control
Chemical Substances	Neuroprotective Agents ; Peptides ; Tat-NR2B9c (D45TI2TWMA)
Language	English
Publishing date	2020-07-01
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	1018059-x
ISSN	1179-1942 ; 0114-5916
ISSN (online)	1179-1942
ISSN	0114-5916
DOI	10.1007/s40264-020-00962-z
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Zs.A 2127: Show issues

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Article ; Online: Assessment of recombinant tissue plasminogen activator (rtPA) toxicity in cultured neural cells and subsequent treatment with poly-arginine peptide R18D.

Kenna, Jade E / Anderton, Ryan S / Knuckey, Neville W / Meloni, Bruno P

Neurochemical research

2020 Volume 45, Issue 5, Page(s) 1215–1229

Abstract: Thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) in ischaemic stroke has been associated with neurotoxicity, blood brain barrier (BBB) disruption and intra-cerebral hemorrhage. To examine rtPA cellular toxicity we investigated ... ...

Abstract	Thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) in ischaemic stroke has been associated with neurotoxicity, blood brain barrier (BBB) disruption and intra-cerebral hemorrhage. To examine rtPA cellular toxicity we investigated the effects of rtPA on cell viability in neuronal, astrocyte and brain endothelial cell (bEnd.3) cultures with and without prior exposure to oxygen-glucose deprivation (OGD). In addition, the neuroprotective peptide poly-arginine-18 (R18D; 18-mer of D-arginine) was examined for its ability to reduce rtPA toxicity. Studies demonstrated that a 4- or 24-h exposure of rtPA was toxic, affecting neuronal cell viability at ≥ 2 µM, and astrocyte and bEnd.3 cells viability at ≥ 5 μM. In addition, a 4-h exposure to rtPA after a period of OGD (OGD/rtPA) exacerbated toxicity, affecting neuronal, astrocyte and bEnd.3 cell viability at rtPA concentrations as low as 0.1 µM. Treatment of cells with low concentrations of R18D (0.5 and 1 µM) reduced the toxic effects of rtPA and OGD/rtPA, while on some occasions a higher 2 µM R18D concentrations exacerbated neuronal and bEnd.3 cell toxicity in OGD/rtPA exposed cultures. In exploratory studies we also demonstrated that OGD activates matrix metalloproteinase-9 (MMP-9) release into the supernatant of astrocyte and bEnd.3 cell cultures, but not neuronal cultures, and that OGD/rtPA increases MMP-9 activation. Furthermore, R18D decreased MMP-9 activation in OGD/rtPA treated astrocyte and bEnd.3 cell cultures. In summary, the findings show that rtPA can be toxic to neural cells and that OGD exacerbates toxicity, while R18D has the capacity to reduce rtPA neural cellular toxicity and reduce MMP-9 activation in astrocytes and bEnd.3. Poly-arginine-18 peptides, which are being developed as neuroprotective therapeutics for ischaemic stroke, therefore have the additional potential of reducing cytotoxic effects associated with rtPA thrombolysis in the treatment of ischaemic stroke.
MeSH term(s)	Animals ; Animals, Newborn ; Cell Survival/drug effects ; Cell Survival/physiology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Intracellular Signaling Peptides and Proteins/pharmacology ; Mice ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/toxicity ; Tissue Plasminogen Activator/toxicity
Chemical Substances	Intracellular Signaling Peptides and Proteins ; R18 peptide ; Recombinant Proteins ; Tissue Plasminogen Activator (EC 3.4.21.68)
Language	English
Publishing date	2020-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-020-03004-3
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