Glial growth factors I-III are specific mitogens for glial cells

Minghetti, Luisa; Goodearl, Andrew; Mistry, K.J.; Stroobant, Paul

doi:10.1002/(sici)1097-4547(19960315)43:6<684::aid-jnr5>3.0.co;2-a

Cited by 31 publications

(15 citation statements)

References 43 publications

(49 reference statements)

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“…The resulting protein was > 98% pure as assessed by reverse‐phase HPLC. Biological activity was confirmed by verifying that recombination factor induced tyrosine phosphorylation of erbB receptors in MCF‐7 breast carcinoma cells and stimulated neonatal Schwann cell proliferation (Minghetti et al . 1996).…”

Section: Methodsmentioning

confidence: 91%

Interactions between β‐neuregulin and neurotrophins in motor neuron apoptosis

Ricart¹,

Pearson²,

Viera³

et al. 2006

Journal of Neurochemistry

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Neuregulins play a major role in the formation and stabilization of neuromuscular junctions, and are produced by both motor neurons and muscle. Although the effects and mechanism of neuregulins on skeletal muscle (e.g. regulation of acetylcholine receptor expression) have been studied extensively, the effects of neuregulins on motor neurons remain unknown. We report that neuregulin-1b (NRGb1) inhibited apoptosis of rat motor neurons for up to 7 days in culture by a phosphatidylinositol 3 kinase-dependent pathway and synergistically enhanced motor neuron survival promoted by glial-derived neurotrophic factor (GDNF). However, binding of neurotrophins, including brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), to the p75 neurotrophin receptor (p75 NTR ) abolished the neuregulin anti-apoptotic effect on motor neurons. Inhibitors of the c-Jun N-terminal kinase (JNK) mitogen-activated protein kinase prevented motor neuron death caused by co-incubation of NRGb1 and BDNF or NGF, as well as by trophic factor deprivation. Motor neuron apoptosis resulting from both trophic factor deprivation and exposure to NRGb1 plus neurotrophins required the induction of neuronal nitric oxide synthase and peroxynitrite formation. Because motor neurons express both p75 NTR and neuregulin erbB receptors during the period of embryonic programmed cell death, motor neuron survival may be the result of complex interactions between trophic and death factors, which may be the same molecules acting in different combinations.

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Section: Methodsmentioning

confidence: 91%

Interactions between β‐neuregulin and neurotrophins in motor neuron apoptosis

Ricart¹,

Pearson²,

Viera³

et al. 2006

Journal of Neurochemistry

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“…Alternative splicing gives rise to various isoforms within each type. For instance, GGF‐I, GGF‐II and GGF‐III at nanomolar concentrations have been shown to be potent mitogens for rat Schwann cells in vitro , whereas at lower concentrations they promote Schwann cell survival (Minghetti et al. 1996).…”

Section: Altered Neurotrophic Factor Expression In Injured Neuronsmentioning

confidence: 99%

Bioengineered nerve regeneration and muscle reinnervation

2006

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The peripheral nervous system has the intrinsic capacity to regenerate but the reinnervation of muscles is often suboptimal and results in limited recovery of function. Injuries to nerves that innervate complex organs such as the larynx are particularly difficult to treat. The many functions of the larynx have evolved through the intricate neural regulation of highly specialized laryngeal muscles. In this review, we examine the responses of nerves and muscles to injury, focusing on changes in the expression of neurotrophic factors, and highlight differences between the skeletal limb and laryngeal muscle systems. We also describe how artificial nerve conduits have become a useful tool for delivery of neurotrophic factors as therapeutic agents to promote peripheral nerve repair and might eventually be useful in the treatment of laryngeal nerve injury.

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“…Because Schwann cell death was measured as a relative density of pyknotic Schwann cells compared with normal, healthy cells, it is possible that the apparent decrease in the level of cell death observed in response to GGF administration could be due to increased proliferation of remaining Schwann cells (Minghetti et al ., 1996; Cheng et al ., 1998). In saline‐treated embryos, the relative density of brachial ventral root Schwann cell mitotic figures was similar to that found in untreated E16.5 mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Although we observed no significant differences in Schwann cell proliferation following GGF treatment, we cannot entirely exclude a proliferative effect on Schwann cell numbers (Maurel & Salzer, 2000). Although neuregulins have been previously identified as mitogens for Schwann cells (Minghetti et al ., 1996; Cheng et al ., 1998; Maurel & Salzer, 2000), this effect is likely dose‐dependent. When cultured Schwann cell precursors are treated with increasing amounts of NDF, an initial survival effect at low doses is superseded by a proliferative response at higher doses (Dong et al ., 1995).…”

Section: Discussionmentioning

confidence: 99%

An in vivo analysis of Schwann cell programmed cell death in embryonic mice: the role of axons, glial growth factor, and the pro‐apoptotic gene Bax

Winseck

Oppenheim

2006

Eur J of Neuroscience

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Building upon previous in vitro studies, the present investigation involves an in vivo examination of Schwann cell programmed cell death (PCD) and development in the brachial spinal ventral roots of embryonic mice. The period of Schwann cell PCD was found to occur between embryonic days (E) 11.5 and 18.5, which is in close coincidence with the PCD period of associated brachial motoneurons (E13.5-E18.5). Additionally, Schwann cells exhibited a peak in proliferation at E11.5, and differentiation from the precursor to the immature Schwann cell stage between E12.5 and E14.5. Axon-mediated Schwann cell survival was demonstrated in vivo by excitotoxic elimination of motoneurons and their axons, via NMDA treatment in utero. This treatment increased apoptotic Schwann cell death within degenerating ventral roots. Conversely, in utero co-treatment of glial growth factor (GGF) with NMDA resulted in decreased Schwann cell death, a finding which supports previous reports of the promotion of Schwann cell survival by GGF. Analysis of mice lacking Bax, a pro-apoptotic Bcl-2 protein, revealed that Schwann cell PCD occurred independently of Bax. However, owing to the lack of motoneuron PCD in Bax-knockout mice, and the corresponding increase in the number of ventral root axons, a decrease in Schwann cell PCD was observed during the normal period of motoneuron PCD. In conclusion, our findings regarding the regulation of Schwann cell development in vivo are consistent with the conclusions from in vitro studies, including a dependency on axons for survival and proliferation signals, timing of differentiation, and a dependency on GGF.

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Glial growth factors I-III are specific mitogens for glial cells

Cited by 31 publications

References 43 publications

Interactions between β‐neuregulin and neurotrophins in motor neuron apoptosis

Interactions between β‐neuregulin and neurotrophins in motor neuron apoptosis

Bioengineered nerve regeneration and muscle reinnervation

An in vivo analysis of Schwann cell programmed cell death in embryonic mice: the role of axons, glial growth factor, and the pro‐apoptotic gene Bax

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