ERK and cell death: ERK1/2 in neuronal death

Subramaniam, Srinivasa; Unsicker, Klaus

doi:10.1111/j.1742-4658.2009.07367.x

Cited by 235 publications

(182 citation statements)

References 71 publications

(83 reference statements)

Supporting

Mentioning

170

Contrasting

Order By: Relevance

“…ERK1/2 is a major mediator of oxidative stress. 24 The western blot data showed that amino-Nogo-A could obviously suppress phosphorylation of ERK2 (p-ERK2) following 5-30 min of H 2 O 2 stimuli (Figure 7a). However, unlike TAT-AM, a specific ERK1/2 inhibitor, U0126 only exhibited a weak neuroprotection (Figures 7b and c).…”

Section: Resultsmentioning

confidence: 99%

Amino-Nogo-A antagonizes reactive oxygen species generation and protects immature primary cortical neurons from oxidative toxicity

Hou

et al. 2012

Cell Death Differ

View full text Add to dashboard Cite

Nogo-A is originally identified as an inhibitor of axon regeneration from the CNS myelin. Nogo-A is mainly expressed by oligodendrocytes, and also by some neuronal subpopulations, particularly in the developing nervous system. Although extensive studies have uncovered regulatory roles of Nogo-A in neurite outgrowth inhibition, precursor migration, neuronal homeostasis, plasticity and neurodegeneration, its cell-autonomous functions in neurons are largely uncharacterized. Here, we show that HIV-1 trans-activating-mediated amino-Nogo-A protein transduction into cultured primary cortical neurons achieves an almost complete neuroprotection against oxidative stress induced by exogenous hydrogen peroxide (H 2 O 2 ). Endogenously expressed neuronal Nogo-A is significantly downregulated upon H 2 O 2 treatment. Furthermore, knockdown of Nogo-A results in more susceptibility to acute oxidative insults and markedly increases neuronal death. Interacting with peroxiredoxin 2 (Prdx2), amino-Nogo-A reduces reactive oxygen species (ROS) generation and extracellular signal-regulated kinase phosphorylation to exert neuroprotective effects. Structure-function mapping experiments reveal that, out of NiG-D20, a novel region comprising residues 290-562 of amino-Nogo-A is indispensable for preventing oxidative neuronal death. Moreover, mutagenesis analysis confirms that cysteine residues 424, 464 and 559 are involved in the inhibition of ROS generation and neuroprotective role of amino-Nogo-A. Our data suggest that neuronal Nogo-A might play a cell-autonomous role in improving neuronal survival against oxidative insult through interacting with Prdx2 and scavenging of ROS.

show abstract

Section: Resultsmentioning

confidence: 99%

Amino-Nogo-A antagonizes reactive oxygen species generation and protects immature primary cortical neurons from oxidative toxicity

Hou

et al. 2012

Cell Death Differ

View full text Add to dashboard Cite

show abstract

“…ERK1/2 is a member of the mitogen-activated protein kinase family that is centrally involved in many processes during the lifetime of a cell. This kinase has been not only associated with proliferation, differentiation, and protection against apoptosis but also has been linked to cell death (37). A selective ERK1/2 inhibitor, FR180204, can protect AMY3 against hAmylin or A␤1-42 toxicity, but this protective effect does not appear to be concentration dependent.…”

Section: Discussionmentioning

confidence: 99%

Amyloid β (Aβ) Peptide Directly Activates Amylin-3 Receptor Subtype by Triggering Multiple Intracellular Signaling Pathways

Ruangkittisakul

MacTavish

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Prosaposin and prosaptides were shown to couple via Gαi and Gαo proteins which are pertussis toxin‐sensitive (Hiraiwa, Campana, Martin, & O'Brien, 1997; Yan, Otero, Hiraiwa, & O'Brien, 2000). The peptides interacted with, at the time, unknown receptors with nanomolar affinity and stimulated ERK phosphorylation (Subramaniam and Unsicker, 2010). Indeed, recently Meyer and colleagues found that GPR37 and GPR37L1 met all these previously established characteristics (Meyer et al, 2013).…”

Section: Potential Therapeutic Targets In Astrocytesmentioning

confidence: 99%

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

Liu

Teschemacher

Kasparov

2017

Glia

View full text Add to dashboard Cite

Astrocytes are key homeostatic cells of the central nervous system. They cooperate with neurons at several levels, including ion and water homeostasis, chemical signal transmission, blood flow regulation, immune and oxidative stress defense, supply of metabolites and neurogenesis. Astroglia is also important for viability and maturation of stem‐cell derived neurons. Neurons critically depend on intrinsic protective and supportive properties of astrocytes. Conversely, all forms of pathogenic stimuli which disturb astrocytic functions compromise neuronal functionality and viability. Support of neuroprotective functions of astrocytes is thus an important strategy for enhancing neuronal survival and improving outcomes in disease states. In this review, we first briefly examine how astrocytic dysfunction contributes to major neurological disorders, which are traditionally associated with malfunctioning of processes residing in neurons. Possible molecular entities within astrocytes that could underpin the cause, initiation and/or progression of various disorders are outlined. In the second section, we explore opportunities enhancing neuroprotective function of astroglia. We consider targeting astrocyte‐specific molecular pathways which are involved in neuroprotection or could be expected to have a therapeutic value. Examples of those are oxidative stress defense mechanisms, glutamate uptake, purinergic signaling, water and ion homeostasis, connexin gap junctions, neurotrophic factors and the Nrf2‐ARE pathway. We propose that enhancing the neuroprotective capacity of astrocytes is a viable strategy for improving brain resilience and developing new therapeutic approaches.

show abstract

ERK and cell death: ERK1/2 in neuronal death

Cited by 235 publications

References 71 publications

Amino-Nogo-A antagonizes reactive oxygen species generation and protects immature primary cortical neurons from oxidative toxicity

Amino-Nogo-A antagonizes reactive oxygen species generation and protects immature primary cortical neurons from oxidative toxicity

Amyloid β (Aβ) Peptide Directly Activates Amylin-3 Receptor Subtype by Triggering Multiple Intracellular Signaling Pathways

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

Contact Info

Product

Resources

About