Increased β-Actin and Tubulin Polymerization in Regrowing Axons: Relationship to the Conditioning Lesion Effect

Lund, Linda M.; Machado, Victor M.; McQuarrie, Irvine G.

doi:10.1006/exnr.2002.8034

Cited by 35 publications

(12 citation statements)

References 24 publications

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“…The increase in mRNA for cytoplasmic β-actin we observed after axotomy is consistent with the increase in β-actin protein expression in DRG neurons reported following sciatic nerve crush and transection (Lund et al 2002). Our data showed that the expression of β-actin was further upregulated by systemic NT-3 administration, suggesting that exogenous NT-3 may stimulate axon growth after axotomy (Young et al 2001).…”

Section: Secreted and Extracellular Moleculessupporting

confidence: 90%

“…Others β-Actin is involved in the transport of cytoplasmic vesicles and is a limiting factor in the speed of axonal outgrowth during regeneration (Lund et al 2002). The increase in mRNA for cytoplasmic β-actin we observed after axotomy is consistent with the increase in β-actin protein expression in DRG neurons reported following sciatic nerve crush and transection (Lund et al 2002).…”

Section: Secreted and Extracellular Moleculessupporting

confidence: 85%

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Gene Expression Profile in Rat Dorsal Root Ganglion Following Sciatic Nerve Injury and Systemic Neurotrophin-3 Administration

et al. 2010

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Following sciatic nerve transection in adult rats, a proportion of injured dorsal root ganglion (DRG) neurons die, through apoptosis, over the following 6 months. Previous studies showed that axotomy and neurotrophin-3 administration may have effects on expression of neurotrophins and their receptors in DRG. In the current study, the fourth and fifth lumbar DRGs of rats were examined 2 weeks after right sciatic nerve transection and ligation. The effects of axotomy and systemic NT-3 treatment on neuronal genes were investigated by microarray. The results demonstrated that bone morphogenetic protein (BMP) and Janus protein tyrosine kinase signaling pathways are induced in axotomized DRG, and PI-3 kinase and BMP pathways and genes controlling various cellular functions were induced after axotomy and NT-3 administration.

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Section: Secreted and Extracellular Moleculessupporting

confidence: 90%

Section: Secreted and Extracellular Moleculessupporting

confidence: 85%

Gene Expression Profile in Rat Dorsal Root Ganglion Following Sciatic Nerve Injury and Systemic Neurotrophin-3 Administration

et al. 2010

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“…Even zymosan, a trigger of robust inflammation, when placed in the vitreous chamber of the eye can stimulate regenerating optic nerve fibers (Leon et al, 2000) and when placed into the DRG before root crush appears essential to the success of DRG regeneration into the spinal cord when combined with modification of the extracellular matrix in the CNS compartment (Steinmetz, et al, 2005). Apparently intense inflammatory states created just outside of the CNS illustrate that in certain circumstances inflammation can promote enhanced regeneration by triggering a conditioning-like effect within the neuron (Calvo et al, 2005;Lund et al, 2002;McQuarrie and Jacob, 1991;Wu et al, 2007a). However, fulminant inflammation centrally tends to create cavities (Fitch, et al, 1999) and it is unclear whether further increasing inflammatory activity, even after attempting to modify immune cell activity, will lead to the desired functional regeneration within the brain and spinal cord (Kigerl et al, 2007;Kigerl et al, 2006;Lazarov-Spiegler et al, 1996;Schwartz and Yoles, 2006).…”

Section: Triggers For the Production Of Inhibitory Extracellular Matrixmentioning

confidence: 99%

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

Fitch

Silver

2008

Experimental Neurology

867

657

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Spinal cord and brain injuries lead to complex cellular and molecular interactions within the central nervous system in an attempt to repair the initial tissue damage. Many studies have illustrated the importance of the glial cell response to injury, and the influences of inflammation and wound healing processes on the overall morbidity and permanent disability that result. The abortive attempts of neuronal regeneration after spinal cord injury are influenced by inflammatory cell activation, reactive astrogliosis and the production of both growth promoting and inhibitory extracellular molecules. Despite the historical perspective that the glial scar was a mechanical barrier to regeneration, inhibitory molecules in the forming scar and methods to overcome them have suggested molecular modification strategies to allow neuronal growth and functional regeneration. Unlike myelin associated inhibitory molecules, which remain at largely static levels before and after central nervous system trauma, inhibitory extracellular matrix molecules are dramatically upregulated during the inflammatory stages after injury providing a window of opportunity for the delivery of candidate therapeutic interventions. While high dose methylprednisolone steroid therapy alone has not proved to be the solution to this difficult clinical problem, other strategies for modulating inflammation and changing the make up of inhibitory molecules in the extracellular matrix are providing robust evidence that rehabilitation after spinal cord and brain injury has the potential to significantly change the outcome for what was once thought to be permanent disability.

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“…With secondary cluster analysis these genes also aligned beside actin-b (ACTB), cofilin-1 (CFL1), myotrophin (V-1 protein) and moesin (Msn), all genes involved in cyoskeletal function. ACTB was originally described as a nonmuscle cytoskeletal actin expressed in a variety of tissues and organs and involved in axon regrowth following injury [40]. A role in kidney disease has not been described previously.…”

Section: Identification Of Cytoskeletal Changes With Cluster Analysismentioning

confidence: 99%

Microarray and bioinformatic detection of novel and established genes expressed in experimental anti-Thy1 nephritis

Sadlier

Ouyang

McMahon

et al. 2005

Kidney International

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Increased β-Actin and Tubulin Polymerization in Regrowing Axons: Relationship to the Conditioning Lesion Effect

Cited by 35 publications

References 24 publications

Gene Expression Profile in Rat Dorsal Root Ganglion Following Sciatic Nerve Injury and Systemic Neurotrophin-3 Administration

Gene Expression Profile in Rat Dorsal Root Ganglion Following Sciatic Nerve Injury and Systemic Neurotrophin-3 Administration

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

Microarray and bioinformatic detection of novel and established genes expressed in experimental anti-Thy1 nephritis

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