Increased expression of mRNAs for microtubule disassembly molecules during nerve regeneration

Iwata, Tatsuya; Namikawa, Kazuhiko; Honma, Masaru; Mori, Nozomu; Yachiku, Sunao; Kiyama, Hiroshi

doi:10.1016/s0169-328x(02)00187-0

Cited by 26 publications

(19 citation statements)

References 28 publications

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“…Indeed, Grenningloh et al (2004) report that overexpression of stathmin, a protein that increases the frequency of microtubule tip catastrophes, increases axon extension. In addition, proteins that regulate microtubule tip dynamics are up regulated during regeneration (Iwata et al, 2002). Second, our results are conceptually consistent with the \push" and \pull" model of axon extension (Letourneau et al, 1987).…”

Section: E14 Axon Extension In the Absence Of F-actin Requires Microtsupporting

confidence: 85%

Developmental regulation of sensory axon regeneration in the absence of growth cones

2006

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The actin filament (F-actin) cytoskeleton is thought to be required for normal axon extension during embryonic development. Whether this is true of axon regeneration in the mature nervous system is not known, but a progressive simplification of growth cones during development has been described and where specifically investigated, mature spinal cord axons appear to regenerate without growth cones. We have studied the cytoskeletal mechanisms of axon regeneration in developmentally early and late chicken sensory neurons, at embryonic day (E) 7 and 14 respectively. Depletion of F-actin blocked the regeneration of E7 but not E14 sensory axons in vitro. The differential sensitivity of axon regeneration to the loss of F-actin and growth cones correlated with endogenous levels of F-actin and growth cone morphology. The growth cones of E7 axons contained more F-actin and were more elaborate than those of E14 axons. The ability of E14 axons to regenerate in the absence of F-actin and growth cones was dependent on microtubule tip polymerization. Importantly, while the regeneration of E7 axons was strictly dependent on F-actin, regeneration of E14 axons was more dependent on microtubule tip polymerization. Furthermore, E14 axons exhibited altered microtubule polymerization relative to E7, as determined by imaging of microtubule tip polymerization in living neurons. These data indicate that the mechanism of axon regeneration undergoes a developmental switch between E7 and E14 from strict dependence on F-actin to a greater dependence on microtubule polymerization. Collectively, these experiments indicate that microtubule polymerization may be a therapeutic target for promoting regeneration of mature neurons.

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Section: E14 Axon Extension In the Absence Of F-actin Requires Microtsupporting

confidence: 85%

Developmental regulation of sensory axon regeneration in the absence of growth cones

2006

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“…Previous studies have demonstrated that stathmin is expressed in mitotically active cells such as cancer cells, crypt cells in the intestinal epithelium, and hepatic epithelial cells after partial hepatectomy (20,23,47,48). Increased expression of stathmin has been shown to be associated with the reentry of the cells into the cell cycle and the onset of cell proliferation (33,34).…”

Section: Discussionmentioning

confidence: 99%

Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure

Zahedi¹,

Wang²,

Barone³

et al. 2004

American Journal of Physiology-Cell Physiology

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“…41 However, RB3 is upregulated in peripheral nerve regeneration 39,42 and SCG10 and SCLIP are induced throughout the sprouting response in peripheral nerve. 44 Similarly, gene expression for p21 and SPRR1 are induced throughout the duration of the peripheral nerve sprouting response 43 unlike their transient induction in the region of poststroke axonal sprouting in peri-infarct cortex. 41 These differences between PNS and CNS postinjury axonal sprouting may reflect true differences in the molecular response of these two systems, and may account for the limited ability of the CNS to sprout.…”

Section: Growth Promotionmentioning

confidence: 99%

Themes and Strategies for Studying the Biology of Stroke Recovery in the Poststroke Epoch

Carmichael

2008

Stroke

105

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Background and Purpose-This review will focus on the emerging principles of neural repair after stroke, and on the overlap between cellular mechanisms of neural repair in stroke and clinical principles of recovery and rehabilitation. Summary of Review-Stroke induces axonal sprouting and neurogenesis. Axonal sprouting occurs in tissue adjacent to the stroke and its connected cortical areas, and from sites that are contralateral to the infarct. Neurogenesis produces newly born immature neurons in peri-infarct striatum and cortex. Stimulation of both axonal sprouting and neurogenesis is associated with improved recovery in animal models of stroke. A unique cellular environment in the poststroke brain supports neural repair: an association of angiogenic and remodeling blood vessels with newly born immature neurons in a neurovasclar niche. Controversies in the field of neural repair after stroke persist, and relate to the locations of axonal sprouting in animal models of stroke and how these correlate to patterns of human remapping and recovery, and to the different models of stroke used in studies of neurogenesis. Conclusions-On a cellular level, the phenomenology of neural repair after stroke has been defined and unique regenerative environments in the poststroke brain identified. As the field moves toward specific studies of causal mechanisms in poststroke repair, it will need to maintain a perspective of the animal models suited to the study of neural repair after stroke as they relate to the patterns of recovery in humans in this disease.

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Increased expression of mRNAs for microtubule disassembly molecules during nerve regeneration

Cited by 26 publications

References 28 publications

Developmental regulation of sensory axon regeneration in the absence of growth cones

Developmental regulation of sensory axon regeneration in the absence of growth cones

Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure

Themes and Strategies for Studying the Biology of Stroke Recovery in the Poststroke Epoch

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