Immunocytochemical evidence for the retrograde transport of intraaxonal cathepsin D: possible relevance to the dying-back process

Sahenk, Zarife; Whitaker, John N.; Mendell, Jerry R.

doi:10.1016/0006-8993(90)90719-r

Cited by 12 publications

(5 citation statements)

References 26 publications

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“…For example, cathepsin D, ninjurin 1, tenascin C and GFRα1 were up‐regulated in the microarray analysis (Fig. 3), consistent with previous reports (Sahenk et al . 1990; Araki and Milbrandt 1996; Baloh et al .…”

Section: Resultssupporting

confidence: 91%

“…For example, cathepsin D, ninjurin 1, tenascin C and GFRa1 were up-regulated in the microarray analysis ( Fig. 3), consistent with previous reports (Sahenk et al 1990;Araki and Milbrandt 1996;Baloh et al 1997;Xiao et al 1997). In addition, almost all myelin-associated proteins like peripheral myelin protein 22 kDa, myelin basic protein, protein zero and periaxin, whose expression was reported to be suppressed during axonal regeneration (Scherer 1997), were also down-regulated in this study (Fig.…”

Section: Resultssupporting

confidence: 91%

“…However, when the nerve was ligated or transected, intra‐axonal cathepsin D appeared as granular or elongated particles and was increased with time at the cut end of the distal stump. In the proximal stump of transected nerves, cathepsin D was detected in the nascent axon tips, as well as in a length of axon extending up to the first node of Ranvier (Sahenk et al . 1990).…”

Section: Discussionmentioning

confidence: 99%

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Analysis of genes induced in peripheral nerve after axotomy using cDNA microarrays

Kubo

Yamashita

Yamaguchi

et al. 2002

Journal of Neurochemistry

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One of the most striking features of neurons in the mature peripheral nervous system is their ability to survive and to regenerate their axons following axonal injury. To perform a comprehensive survey of the molecular mechanisms that underlie peripheral nerve regeneration, we analyzed a cDNA library derived from the distal stumps of post-injured sciatic nerve which was enriched in non-myelinating Schwann cells using cDNA microarrays. The number of up-and down-regulated genes in the transected sciatic nerve was 370 and 157, respectively, of the 9596 spotted genes. In the up-regulated group, the number of known genes was 216 and the number of expressed sequence tag (EST) sequences was 154. In the down-regulated group, the number of known genes was 103 and that of EST sequences was 54. We obtained several genes that were previously reported to be involved in regeneration of the injured neurons, such as cathepsin D, ninjurin 1, tenascin C, and co-receptor for glial cell line-derived neurotrophic factor family of trophic factors. In addition to unknown genes, there seemed to be a lot of annotated genes whose role in nerve regeneration remains unknown. Keywords: cDNA microarrays, injury-induced molecules, nerve regeneration, Schwann cell, sciatic nerve. One of the most striking features of neurons in the mature PNS is their ability to survive and to regenerate their axons following axonal injury. It has been increasingly evident that the success of axonal regeneration is dependent on the intrinsic as well as extrinsic growth properties of the axotomized neuron. The environment in which PNS axons regenerate consists of Schwann cells and their basal laminae, fibroblasts, collagen, degenerating myelin and phagocytic cells (Fawcett and Keynes 1990;Bunge and Griffin 1992;Araki and Milbrandt 1996). After nerve injury, the distal axonal and myelin segment undergoes dissolution and absorption by the surrounding cellular environment, a process called Wallerian degeneration. Then, the remaining Schwann cells divide and align longitudinally within basal lamina tubes. Growth cones from regenerating axons extend along the Schwann cell bands (the band of Bü ngner), growing along the Schwann cell membranes and basal laminae (Keynes 1987;Reichert et al. 1994;Grill and Tuszynske 1999). Such biological and morphological changes of Schwann cells are thought to be controlled by injury-induced molecules that are expressed by neurons and Schwann cells themselves. Especially, at around 7 days after nerve injury, many nerve regeneration-related factors, such as p75 NTR , co-receptor for glial cell line-derived neurotrophic factor family of trophic factors (GFRa1) and ninjurin 1 and 2, reach peak levels (Taniuchi et al. 1988;Araki and Milbrandt 1996;Baloh et al. 1997;Araki and Milbrandt 2000), and the growth cones of regenerating axons begin to move over the Schwann cell surface (Taniuchi et al. 1988;Goodrum et al. 1994). Successive large-scale screening, however, is required to reveal the spectrum of genes involved in this regenerat...

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Section: Resultssupporting

confidence: 91%

Section: Resultssupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Analysis of genes induced in peripheral nerve after axotomy using cDNA microarrays

Kubo

Yamashita

Yamaguchi

et al. 2002

Journal of Neurochemistry

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“…Similarly, electron microscopy of hippocampal slices showed that lysosomes were essentially confined to cell bodies (32). Moreover, lysosomal proteases, such as cathepsin D, are normally absent from axons (33), and in sympathetic neurons, cholesterol hydrolase activity was detected only in cell bodies (B. Karten and J. E. Vance, unpublished observations). Our previous work demonstrated that in mouse sympathetic neurons, NPC1 is present not only in neuronal cell bodies in late endosomes and lysosomes but is also abundant in vesicular structures in distal axons (23).…”

Section: Npc1 Is Present In Distal Axons Of Sympathetic Neurons and Cmentioning

confidence: 93%

The Niemann-Pick C1 protein in recycling endosomes of presynaptic nerve terminals

Karten

Campenot

Vance

et al. 2006

Journal of Lipid Research

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Niemann-Pick type C (NPC) disease is a fatal, neurodegenerative disorder caused in 95% of cases by loss of function of NPC1, a ubiquitous endosomal transmembrane protein. A biochemical hallmark of NPC deficiency is cholesterol accumulation in the endocytic pathway. Although cholesterol trafficking defects are observed in all cell types, neurons are the most vulnerable to NPC1 deficiency, suggesting a specialized function for NPC1 in neurons. We investigated the subcellular localization of NPC1 in neurons to gain insight into the mechanism of action of NPC1 in neuronal metabolism. We show that NPC1 is abundant in axons of sympathetic neurons and is present in recycling endosomes in presynaptic nerve terminals. NPC1 deficiency causes morphological and biochemical changes in the presynaptic nerve terminal. Synaptic vesicles from Npc1 2/2 mice have normal cholesterol content but altered protein composition. We propose that NPC1 plays a previously unrecognized role in the presynaptic nerve terminal and that NPC1 deficiency at this site might contribute to the progressive neurological impairment in NPC disease.-Karten, B., R. B. Campenot, D. E. Vance, and J. E. Vance. The Niemann-Pick C1 protein in recycling endosomes of presynaptic nerve terminals. J. Lipid Res. 2006. 47: 504-514.

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“…Within the nervous system, Cat-S is expressed mainly in microglial cells and macrophages and in low levels in DRG neurons (Barclay et al, 2007). However, Cat-S and other cathepsins are upregulated in sensory neuron axons and Schwann cells after nerve ligation or neurotoxic exposure (Kubo et al, 2002;Sahenk et al, 1990;Whitaker et al, 1983). Similarly, human KCs can display a striking Cat-S activity after stimulation (Schwarz et al, 2002).…”

Section: Cat-s As a Molecular Link Between Na V And Par2 Activation Elicited By P-ctx-2mentioning

confidence: 99%

PAR2, Keratinocytes, and Cathepsin S Mediate the Sensory Effects of Ciguatoxins Responsible for Ciguatera Poisoning

L’Hérondelle

Pierre

Fouyet

et al. 2021

Journal of Investigative Dermatology

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Immunocytochemical evidence for the retrograde transport of intraaxonal cathepsin D: possible relevance to the dying-back process

Cited by 12 publications

References 26 publications

Analysis of genes induced in peripheral nerve after axotomy using cDNA microarrays

Analysis of genes induced in peripheral nerve after axotomy using cDNA microarrays

The Niemann-Pick C1 protein in recycling endosomes of presynaptic nerve terminals

PAR2, Keratinocytes, and Cathepsin S Mediate the Sensory Effects of Ciguatoxins Responsible for Ciguatera Poisoning

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