Steven Petratos

ORCID: 0000-0003-1211-4577
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About
Contact & Profiles
Research Areas
  • Neurogenesis and neuroplasticity mechanisms
  • Nerve injury and regeneration
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Multiple Sclerosis Research Studies
  • Axon Guidance and Neuronal Signaling
  • Peripheral Neuropathies and Disorders
  • Alzheimer's disease research and treatments
  • Spinal Cord Injury Research
  • Hereditary Neurological Disorders
  • Thyroid Disorders and Treatments
  • Signaling Pathways in Disease
  • Herpesvirus Infections and Treatments
  • RNA Interference and Gene Delivery
  • Mitochondrial Function and Pathology
  • Neuroblastoma Research and Treatments
  • Immune Cell Function and Interaction
  • Congenital heart defects research
  • Glycosylation and Glycoproteins Research
  • S100 Proteins and Annexins
  • Pluripotent Stem Cells Research
  • HIV Research and Treatment
  • RNA regulation and disease
  • Cell death mechanisms and regulation
  • Hippo pathway signaling and YAP/TAZ
  • Cholinesterase and Neurodegenerative Diseases

Monash University
2015-2024

Nelson Mandela University
2024

Australian Regenerative Medicine Institute
2020-2021

The University of Western Australia
2015

Hudson Institute of Medical Research
2015

The University of Sydney
2015

Inserm
2015

Sorbonne Université
2015

Institut du Cerveau
2015

Centre National de la Recherche Scientifique
2015

Neuritic abnormalities are a major hallmark of Alzheimer's disease (AD) pathology. Accumulation β-amyloid protein (Aβ) in the brain causes changes neuritic processes individuals with this disease. In study, we show that Aβ decreases neurite outgrowth from SH-SY5Y human neuroblastoma cells. To explore molecular pathways by which alters outgrowth, examined activation and localization RhoA Rac1 regulate level phosphorylation collapsin response mediator protein-2 (CRMP-2). increased levels...

10.1093/brain/awm260 article EN Brain 2007-11-13

Multiple sclerosis involves demyelination and axonal degeneration of the central nervous system. The molecular mechanisms are relatively unexplored in both multiple its mouse model, experimental autoimmune encephalomyelitis. We previously reported that targeting growth inhibitor, Nogo-A, may protect against neurodegeneration encephalomyelitis; however, mechanism by which this occurs is unclear. now show collapsin response mediator protein 2 (CRMP-2), an important tubulin-associated regulates...

10.1093/brain/aws100 article EN Brain 2012-04-28

Schwann cells express the low-affinity neurotrophin receptor (p75), but no role for either neurotrophins or their cognate receptors in cell development has been established. We have found that isolated from postnatal day 1 (P1) P2 mice were p75-deficient exhibited potentiated survival compared to wild-type after growth factor and serum withdrawal. There was, however, disparity of at embryonic 15, suggesting death-inducing effects p75 are developmentally regulated. A comparable degree death...

10.1523/jneurosci.20-15-05741.2000 article EN cc-by-nc-sa Journal of Neuroscience 2000-08-01

Abstract Re‐expression of the death‐signalling p75 neurotrophin receptor (p75 NTR ) is associated with injury and neurodegeneration in adult nervous system. The induction expression mature degenerating spinal motor neurons humans transgenic mice amyotrophic lateral sclerosis (ALS) suggests a role progression neuron disease (MND). In this study, we designed, synthesized evaluated novel antisense peptide nucleic acid (PNA) constructs targeting as potential gene knockdown therapeutic strategy...

10.1046/j.1471-4159.2003.02053.x article EN Journal of Neurochemistry 2003-10-02

As a consequence of secondary pathophysiological mechanisms elicited after spinal cord injury (SCI), oligodendrocytes die by waves apoptosis. This ultimately results in demyelination intact axons leading to loss their conducting properties. Preservation as few 5% 10% myelinated individual tracts can confer locomotor recovery. Thus, strategies aimed at rescuing mature ensheathing viable are likely be therapeutic significance. We report that leukemia inhibitory factor (LIF) prevent...

10.1097/01.jnen.0000235855.77716.25 article EN Journal of Neuropathology & Experimental Neurology 2006-09-01

Brain and spinal cord injuries present significant therapeutic challenges. The treatments available for these conditions are largely ineffective, partly due to limitations in directly targeting the agents sites of pathology within central nervous system (CNS). use stem cells treat presents a novel strategy. A variety cell have been examined animal models CNS trauma. Many studies used as cell-replacement These investigations also highlighted this approach. Another potential strategy therapy...

10.2174/157015910793358204 article EN Current Neuropharmacology 2010-11-16

Cell membrane thyroid hormone (TH) transport can be facilitated by the monocarboxylate transporter 8 (MCT8), encoded solute carrier family 16 member 2 (SLC16A2) gene. Human mutations of gene, SLC16A2, result in X-linked-inherited psychomotor retardation and hypomyelination disorder, Allan-Herndon-Dudley syndrome (AHDS). We posited that abrogating MCT8-dependent TH limits oligodendrogenesis myelination. show human oligodendrocytes (OL), derived from NKX2.1-GFP embryonic stem cell (hESC)...

10.1016/j.ebiom.2017.10.016 article EN cc-by-nc-nd EBioMedicine 2017-10-19

An imbalance in oxidative stress and antioxidant defense mechanisms contributes to the development of ischaemic retinopathies such as diabetic retinopathy prematurity (ROP). Currently, therapeutic utility targeting key transcription factors restore this remains be determined. We postulated that dh404, an activator nuclear factor erythroid-2 related 2 (Nrf2), master regulator responses, would attenuate retinal vasculopathy by involving protection against stress-mediated damage glia....

10.1042/cs20160068 article EN Clinical Science 2016-03-23

Abstract Transthyretin (TTR) is a protein that binds and distributes thyroid hormones (THs) in blood cerebrospinal fluid. Previously, two reports identified TTR null mice as hypothyroid the central nervous system (CNS). This prompted our investigations into developmentally regulated TH-dependent processes brains of wildtype mice. Despite logical expectations hypomyelinating phenotype CNS mice, we observed hypermyelination phenotype, synchronous with an increase density oligodendrocytes...

10.1038/s41598-020-60699-8 article EN cc-by Scientific Reports 2020-03-06

Abstract Precursor cells have the capacity to repopulate demyelinated brain, but molecular mechanisms that facilitate their recruitment are largely unknown. The low‐affinity neurotrophin receptor, p75 NTR , may be one of these regulators; however, its expression profile by oligodendroglia within multiple sclerosis (MS) brain remains uncertain. We therefore assessed this receptor 8 MS and 4 control brains. found no evidence mature oligodendrocytes. Instead, we demonstrated presence on a...

10.1002/glia.20056 article EN Glia 2004-05-26

Neurodegenerative diseases, such as multiple sclerosis represent global health issues. Accordingly, there is an urgent need to understand the pathogenesis of this and other central nervous system disorders, so that more effective therapeutics can be developed. Cerebrospinal fluid a potential source important reporter molecules released from various cell types result pathology. Here, we report development unbiased approach for detection reactive cerebrospinal target brain proteins patients...

10.1074/mcp.m110.000042 article EN cc-by Molecular & Cellular Proteomics 2011-03-19
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