Regulation of Caspases in the Nervous System

Troy, Carol M.; Akpan, Nsikan; Jean, Ying Y.

doi:10.1016/b978-0-12-385504-6.00007-5

Cited by 50 publications

(21 citation statements)

References 246 publications

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“…caspases 3, 6, 7) [47]. However, the conservation and modulation of these apoptotic pathways across pathophysiological stimuli and photoreceptor degenerations remain controversial [43, 48–53]. Hence, we extended the analysis of the modulatory role of CLDm of Ranbp2 in cell death by examining the activation of initiator and effector caspases in cell bodies of photoreceptors.…”

Section: Resultsmentioning

confidence: 99%

Uncoupling phototoxicity‐elicited neural dysmorphology and death by insidious function and selective impairment of Ran‐binding protein 2 (Ranbp2)

et al. 2015

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Morphological disintegration of neurons is coupled invariably to neural death. In particular, disruption of outer segments of photoreceptor neurons triggers photoreceptor death regardless of the pathological stressors. We show that Ranbp2−/−::Tg-Ranbp2CLDm mice with mutations in SUMO-binding motif (SBM) of cyclophilin-like domain (CLD) of Ranbp2 expressed in a null Ranbp2 background lack untoward effects in photoreceptors in the absence of light-stress. However, compared to wild type photoreceptors, light-stress elicits profound disintegration of outer segments of Ranbp2−/−::Tg-Ranbp2CLDm with paradoxical age-dependent resistance of photoreceptors to death and genotype-independent caspase activation. Ranbp2−/−::Tg-Ranbp2CLDm exhibit photoreceptor death-independent changes in ubiquitin-proteasome system (UPS), but death-dependent increase of ubc9 levels. Hence, insidious functional impairment of SBM of Ranbp2’s CLD promotes neuroprotection and uncoupling of photoreceptor degeneration and death against phototoxicity.

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Section: Resultsmentioning

confidence: 99%

Uncoupling phototoxicity‐elicited neural dysmorphology and death by insidious function and selective impairment of Ran‐binding protein 2 (Ranbp2)

et al. 2015

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“…Caspases can be divided into three groups: initiator caspases (caspase-2, -8, -9, -10), effector caspases (caspase-3, -6, -7), and inflammatory caspases (caspase-1, -4, -5, -11, -12). Whereas effector caspases are activated by the initiator caspases, initiator caspases are activated by different, more complex mechanisms [54]. …”

Section: The Role Of Caspases In Neonatal Brain Injurymentioning

confidence: 99%

Molecular Mechanisms of Neonatal Brain Injury

Thornton

Rousset

Kichev

et al. 2012

Neurology Research International

108

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Fetal/neonatal brain injury is an important cause of neurological disability. Hypoxia-ischemia and excitotoxicity are considered important insults, and, in spite of their acute nature, brain injury develops over a protracted time period during the primary, secondary, and tertiary phases. The concept that most of the injury develops with a delay after the insult makes it possible to provide effective neuroprotective treatment after the insult. Indeed, hypothermia applied within 6 hours after birth in neonatal encephalopathy reduces neurological disability in clinical trials. In order to develop the next generation of treatment, we need to know more about the pathophysiological mechanism during the secondary and tertiary phases of injury. We review some of the critical molecular events related to mitochondrial dysfunction and apoptosis during the secondary phase and report some recent evidence that intervention may be feasible also days-weeks after the insult.

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“…Activation of caspases occurs during apoptosis [89,162,163]. In the extrinsic pathway, the intracellular death domain of death receptors, such as the tumor necrosis family (TNF) superfamily, Fas/CD95/Apo-1, can bind to extracellular ligands and lead to an intracellular death-inducing signaling complex following recruitment of adaptor molecules, such as the Fas associated death domain (FADD).…”

Section: Epo Oxidative Stress and Apoptosismentioning

confidence: 99%

Erythropoietin: New Directions for the Nervous System

Maiese

Chong

Shang

et al. 2012

IJMS

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New treatment strategies with erythropoietin (EPO) offer exciting opportunities to prevent the onset and progression of neurodegenerative disorders that currently lack effective therapy and can progress to devastating disability in patients. EPO and its receptor are present in multiple systems of the body and can impact disease progression in the nervous, vascular, and immune systems that ultimately affect disorders such as Alzheimer’s disease, Parkinson’s disease, retinal injury, stroke, and demyelinating disease. EPO relies upon wingless signaling with Wnt1 and an intimate relationship with the pathways of phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), and mammalian target of rapamycin (mTOR). Modulation of these pathways by EPO can govern the apoptotic cascade to control β-catenin, glycogen synthase kinase-3β, mitochondrial permeability, cytochrome c release, and caspase activation. Yet, EPO and each of these downstream pathways require precise biological modulation to avert complications associated with the vascular system, tumorigenesis, and progression of nervous system disorders. Further understanding of the intimate and complex relationship of EPO and the signaling pathways of Wnt, PI 3-K, Akt, and mTOR are critical for the effective clinical translation of these cell pathways into robust treatments for neurodegenerative disorders.

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Regulation of Caspases in the Nervous System

Cited by 50 publications

References 246 publications

Uncoupling phototoxicity‐elicited neural dysmorphology and death by insidious function and selective impairment of Ran‐binding protein 2 (Ranbp2)

Uncoupling phototoxicity‐elicited neural dysmorphology and death by insidious function and selective impairment of Ran‐binding protein 2 (Ranbp2)

Molecular Mechanisms of Neonatal Brain Injury

Erythropoietin: New Directions for the Nervous System

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