wallerian degeneration/protease

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The Complex Work of Proteases and Secretases in Wallerian Degeneration: Beyond Neuregulin-1.

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After damage, axons in the peripheral nervous system (PNS) regenerate and regrow following a process termed Wallerian degeneration, but the regenerative process is often incomplete and usually the system does not reach full recovery. Key steps to the creation of a permissive environment for axonal

Pathogenesis of axonal degeneration: parallels between Wallerian degeneration and vincristine neuropathy.

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Peripheral neuropathies and Wallerian degeneration share a number of pathological features; the most prominent of which is axonal degeneration. We asked whether common pathophysiologic mechanisms are involved in these 2 disorders by directly comparing in vitro models of axonal degeneration after

Endoneurial remodeling by TNFalph- and TNFalpha-releasing proteases. A spatial and temporal co-localization study in painful neuropathy.

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Peripheral nerve injury causing Wallerian degeneration results in endoneurial remodeling initiated by an increase in tumor necrosis factor-alpha (TNF), which is activated from its precursor by extracellular proteases of the matrix metalloproteinase (MMP) family. We used immunohistochemistry to

Plasminogen activators in rat neural tissues during development and in Wallerian degeneration.

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The fibrinolytic activity of blood is caused by plasminogen activators (PA) converting plasminogen to plasmin, the active fibrinolytic protease. PA activity in rat neural tissues was studied by Todd's fibrin slide technique. Cryostat sections overlayed with a film of plasminogen and fibrin were

Very early activation of m-calpain in peripheral nerve during Wallerian degeneration.

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Peripheral nerve injury results in a series of events culminating in degradation of the axonal cytoskeleton (Wallerian degeneration). In the time period between axotomy and cytoskeletal degradation (24-48 h in rodents), there is calcium entry and activation of calpains within the axon. The precise

N-alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) suppresses neuritic degeneration caused by different experimental paradigms including in vitro Wallerian degeneration.

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Accumulating evidence indicates that neurite degeneration occurs via a distinct mechanism from somal death programs. We have previously shown that neuritic ATP level in sympathetic neurons decreases, whereas somal ATP level remains unaltered during degeneration caused by the microtubule-disrupting

Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation do not involve caspases.

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The selective degeneration of an axon, without the death of the parent neuron, can occur in response to injury, in a variety of metabolic, toxic, and inflammatory disorders, and during normal development. Recent evidence suggests that some forms of axon degeneration involve an active and regulated

Calpains mediate axonal cytoskeleton disintegration during Wallerian degeneration.

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In both the central nervous system (CNS) and peripheral nervous system (PNS), transected axons undergo Wallerian degeneration. Even though Augustus Waller first described this process after transection of axons in 1850, the molecular mechanisms may be shared, at least in part, by many human

Loss of the compound action potential: an electrophysiological, biochemical and morphological study of early events in axonal degeneration in the C57BL/Ola mouse.

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In the C57BL/Ola (Ola) mouse strain there is a marked slowing of axonal disintegration during Wallerian degeneration. The locus of the mutation controlling this phenomenon (slow Wallerian degeneration--Wlds) has been mapped to chromosome 4, and its protective effect decreases with advancing age.

Calpain-mediated cleavage of collapsin response mediator protein(CRMP)-2 during neurite degeneration in mice.

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Axon or dendrite degeneration involves activation of the ubiquitin-proteasome system, failure to maintain neuritic ATP levels, microtubule fragmentation and a mitochondrial permeability transition that occur independently of the somal death programs. To gain further insight into the neurite

Distribution of calpains I and II in rat brain.

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Calpains I and II are calcium-dependent proteases that have been implicated in several aspects of brain function, including neurofilament turnover, Wallerian degeneration, and excitatory synaptic transmission. In this study, specific affinity-purified antibodies against each of the enzymes were used

Calcium-mediated degeneration of the axonal cytoskeleton in the Ola mouse.

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The C57BL/Ola (Ola) mouse is a mutant substrain in which transected axons undergo very slow Wallerian degeneration. Because axonal degradation during Wallerian degeneration is calcium dependent, we tested whether Ola axons are susceptible to calcium-mediated axonal degeneration by comparing

Axonal neurofilaments are resistant to calpain-mediated degradation in the WLD(S) mouse.

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The biological basis for the phenotype of delayed Wallerian degeneration in the WLDs mouse has yet to be elucidated, although it is known that the characteristic is intrinsic to the axon. Previous data suggested that nerves from the WLD(S) are relatively resistant to proteolytic degradation. We

Inhibition of neural and muscle degeneration after epineural neurorrhaphy.

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Investigations were undertaken on the regeneration of transected rat sciatic nerves. The ability of the protease inhibitor leupeptin to inhibit wallerian degeneration and muscle atrophy was evaluated. After transection of a sciatic nerve and immediate neurorrhaphy, animals were treated with

Calpain inhibitor 2 prevents axonal degeneration of opossum optic nerve fibers.

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The ultrastructural change that characterizes the onset of Wallerian degeneration is the disintegration of axoplasmic microtubules and neurofilaments, which are converted into an amorphous and granular material, followed by myelin breakdown. The mechanism underlying such processes is an increase in

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