Reduced NGF secretion by Schwann cells under the high glucose condition decreases neurite outgrowth of DRG neurons

Tosaki, Takahiro; Kawanishi, Hideki; Yasuda, Yutaka; Naruse, Keiko; Kato, Koichi; Kozakae, Mika; Nakamura, Nobuhisa; Shibata, Tsutomu; Hamada, Yoji; Nakashima, Eitaro; Oiso, Yutaka; Nakamura, Jiro

doi:10.1016/j.expneurol.2008.06.017

Cited by 68 publications

(44 citation statements)

References 39 publications

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“…It has been suggested that internal ribosomal initiation of mRNA translation, a step that is affected by rapamycin and p70S6K, is critical for survival of cells under transient apoptotic stress ( 107 ). Postmitotic neurons require protein synthesis for survival ( 108 ) so it is possible that insulin stimulates protein synthesis via a rapamycin-dependent ture, are consistent with reports showing impaired axonal growth and aberrant dystrophic structures in dorsal root ganglion neurons from diabetic animals and in neurons cultured under high glucose conditions ( 154,155 ).…”

Section: Protein Tyrosine Phosphatase-1b and Pi3k Pathwaysupporting

confidence: 58%

Phosphoinositide 3-kinase signaling in the vertebrate retina

Rajala

2010

Journal of Lipid Research

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This article is available online at http://www.jlr.org was established by Streb et al. ( 3 ) in their classic paper that showed elevations in IP 3 caused intracellular release of bound calcium. Subsequently, 1,2-DG was found to stimulate protein kinase C (PKC), a serine/threonine kinase that phosphorylates a number of cellular proteins ( 4 ). Activation of the PLC/PKC cascade affects a variety of cellular events, including secretion, phagocytosis, smooth muscle contraction, proliferation, neurotransmission, and metabolism [see reviews by Rhee ( 5 ), Rhee and Choi ( 6 ), and Berridge ( 7 ) THE PI CYCLEIn the early 1950s, Hokin and Hokin ( 1, 2 ) discovered that addition of acetylcholine to brain slices stimulated the incorporation of phosphate and inositol but not glycerol into lipids; the major products of this incorporation were phosphatidylinositol (PI) and phosphatidic acid. Subsequent studies defi ned the reactions of the PI cycle and showed that the initial event was receptor-meditated activation of a phospholipase C (PLC), which hydrolyzes phosphatidylinositol 4,5-bisphosphate (PI-4,5-P 2 ) to 1,2-diacylglycerol (DG) and inositol 1,4,5-trisphosphate (IP 3 ). This increase in lipid synthesis reported by the Hokins was a recovery reaction that rapidly replenished PI separate from de novo PI synthesis. The role of 1,4, This work was supported by grants

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Section: Protein Tyrosine Phosphatase-1b and Pi3k Pathwaysupporting

confidence: 58%

Phosphoinositide 3-kinase signaling in the vertebrate retina

Rajala

2010

Journal of Lipid Research

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“…In mice with peripheral neuropathy, NGF promoted the recovery of peripheral nerves (45). Schwann cells are known to release NGF and promote DRG neuron axonal growth by secreting NGF (46), and thus, Schwann cell dysfunction affects the survival, maintenance, and differentiation of peripheral nerves. The adhesion of Schwann cells to extracellular matrix is crucial for peripheral nerve morphogenesis, growth, and myelination, and mutations in laminin or integrin subunit in Schwann cells have been shown to cause inherited peripheral neuropathy (47,48).…”

Section: Discussionmentioning

confidence: 99%

Axonal Neuropathy-associated TRPV4 Regulates Neurotrophic Factor-derived Axonal Growth

Jang

Jung

Kim

et al. 2012

Journal of Biological Chemistry

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Background:Because genetic linkage studies identified mutations in TRPV4 in patients with peripheral neuropathies, the function of TRPV4 in peripheral neurons is questioned. Results: TRPV4 was found to promote neurotrophic factor-driven neuritogenesis. Conclusion: TRPV4 mediates neurotrophic factor-driven neuritogenesis in peripheral neurons. Significance: This explains molecular mechanisms underlying neuritogenesis and maintenance of peripheral nerves.

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“…After traumatic injury to a nerve, reciprocal signalling normally occurs between the axon and glia, and this signalling is necessary for the reformation of the myelin-axon unit during regeneration. Compromised Schwann cell production of the neurotrophic factors NGF and NT-3 that are essential to nerve structure and function is linked to the loss of glia-axon associations and decreased neurite outgrowth, suggesting that reduced production of these factors by Schwann cells has an important role in impaired axonal regeneration 21,155,156 . Indeed, after experimental axotomy, Schwann cell growth was robust and extended into the superficial dermis in people without diabetic neuropathy, whereas people with injury as a result of diabetes exhibited atrophic Schwann tubes that were limited to the mid-dermis, and limited regenerative axonal sprouting 157 .…”

Section: Impact Of Schwannopathy On Neuronsmentioning

confidence: 99%

Schwann cell interactions with axons and microvessels in diabetic neuropathy

et al. 2017

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The incidence of diabetes mellitus has increased dramatically over the past two to three decades. According to the International Diabetes Federation Diabetes Atlas, 415 million people worldwide had diabetes in 2015, and this number is expected to grow by 5% annually, predominantly as a result of increasing prevalence of type 2 diabetes. Furthermore, an estimated 100 million Europeans and 80 million Americans have impaired glucose tolerance or prediabetes. Few people die from acute diabetes in countries with comprehensive health care systems, but the disease is inflicting a huge medical, social and economic burden on society owing to the need for lifelong treatment of its systemic consequences and the insidious development of multi-organ damage.Peripheral neuropathy (BOXES 1,2) is a common but often neglected complication of long-term diabetes, and the lack of treatment options reflects an incomplete understanding of the pathogenic mechanisms. Hyperglycaemia is generally accepted as the primary pathogenic insult in type 1 and type 2 diabetic neuropathy, although roles are emerging for other factors, such as impaired insulin signalling, hypertension and dyslipidaemia (particularly for type 2 diabetes), which might precede overt hyperglycaemia 1 . Many preclinical studies, and occasional clinical studies, have indicated that diabetic neuropathy -like diabetic nephropathy and retinopathy -results from microvascular disease, with a focus on axonal degeneration as a consequence of ischaemia and/or hypoxia. This mechanism, however, is likely to be only one aspect of a more complex pathogenesis.The earliest descriptions of pathology in diabetic neuropathy indicated that Schwannopathy accompanied axonal degeneration. The majority of clinical and basic research in diabetic neuropathy since then has focused on the effects on neurons. However, accumulating data from research into the development and regeneration of the PNS has identified Schwann cells as equally indispensable components that maintain neuronal structure and function, nourish axons, and promote survival and growth upon injury. The early reports from 1979 that demonstrated morphological changes in Schwann cells in human diabetic neuropathy 2 are now supported by an increased awareness of molecular alterations in Schwann cells during diabetes 3 . Schwann cells express a wide range of receptors and, when they sense insults or danger signals, they upregulate synthesis and secretion of factors that stimulate neuroprotection, regrowth and remyelination, or factors that aggravate disease phenotypes 4 . The most recent studies have demonstrated that Schwann cells regulate many aspects of axonal function, so that disruption of their metabolism by diabetes results in the accumulation of neurotoxic intermediates and compromises production of neuronal support factors, contributing to axonal degeneration, endothelial dysfunction and diabetic neuropathy. Abstract | The prevalence of diabetes worldwide is at pandemic levels, with the number of patients increasing by 5% annu...

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Reduced NGF secretion by Schwann cells under the high glucose condition decreases neurite outgrowth of DRG neurons

Cited by 68 publications

References 39 publications

Phosphoinositide 3-kinase signaling in the vertebrate retina

Phosphoinositide 3-kinase signaling in the vertebrate retina

Axonal Neuropathy-associated TRPV4 Regulates Neurotrophic Factor-derived Axonal Growth

Schwann cell interactions with axons and microvessels in diabetic neuropathy

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