E‐cadherin expression in postnatal Schwann cells is regulated by the cAMP‐dependent protein kinase a pathway

Crawford, Audrita T.; Desai, Darshan; Gokina, Pradeepa; Basak, Samar; Kim, Haesun A.

doi:10.1002/glia.20716

Cited by 29 publications

(29 citation statements)

References 39 publications

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“…In keratinocytes, merlin also associates with adherens junctions, where it interacts with complexes of E-cadherin and β-catenin [99]. Wild-type Schwann cells express both E-cadherin [33,129,209] and N-cadherin [107,190,191]; consistent with the findings delineated above, loss of merlin results in disruption of adherens junctions in primary cultures of schwannoma cells [53]. …”

Section: Schwannomasmentioning

confidence: 59%

Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms

Carroll

2011

Acta Neuropathol

107

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Neurofibromas, schwannomas and malignant peripheral nerve sheath tumors (MPNSTs) all arise from the Schwann cell lineage. Despite their common origin, these tumor types have distinct pathologies and clinical behaviors; a growing body of evidence indicates that they also arise via distinct pathogenic mechanisms. Identification of the genes that are mutated in genetic diseases characterized by the development of either neurofibromas and MPNSTs [neurofibromatosis type 1 (NF1)] or schwannomas [neurofibromatosis type 2 (NF2), schwannomatosis and Carney complex type 1] has greatly advanced our understanding of these mechanisms. The development of genetically engineered mice with ablation of NF1, NF2, SMARCB1/INI1 or PRKAR1A has confirmed the key role these genes play in peripheral nerve sheath tumorigenesis. Establishing the functions of the NF1, NF2, SMARCB1/INI1 and PRKAR1A gene products has led to the identification of key cytoplasmic signaling pathways promoting Schwann cell neoplasia and identified new therapeutic targets. Analyses of human neoplasms and genetically engineered mouse models have established that interactions with other tumor suppressors such as TP53 and CDKN2A promote neurofibroma-MPNST progression and indicate that intratumoral interactions between neoplastic and non-neoplastic cell types play an essential role in peripheral nerve sheath tumorigenesis. Recent advances have also provided new insights into the identity of the neural crest-derived populations that give rise to different types of peripheral nerve sheath tumors. Based on these findings, we now have an initial outline of the molecular mechanisms driving the pathogenesis of neurofibromas, MPNSTs and schwannomas. However, this improved understanding in turn raises a host of intriguing new questions.

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Section: Schwannomasmentioning

confidence: 59%

Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms

Carroll

2011

Acta Neuropathol

107

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“…E-cadherin maintains the structural integrity of non-compact myelin domains in vivo (Perrin-Tricaud et al 2007; Young et al 2002). cAMP regulates E-cadherin in postnatal SCs (Crawford et al 2008). Notably, cAMP can act downstream of Rac1 in mouse embryonic fibroblast cells (Chen et al 2008), and cAMP is critical for SC myelination (Arthur-Farraj et al 2011; Monk et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Rac1 Controls Schwann Cell Myelination through cAMP and NF2/merlin

Moon

Niehaus

et al. 2012

J. Neurosci.

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During peripheral nervous system development, Schwann cells (SCs) surrounding single large axons differentiate into myelinating SCs. Previous studies implicate RhoGTPases in SC myelination, but the mechanisms involved in RhoGTPase regulation of SC myelination are unknown. Here, we show that SC myelination is arrested in Rac1 conditional knockout (Rac1-CKO) mice. Rac1 knockout abrogated phosphorylation of the effector p21-activated kinase (PAK) and decreased NF2/merlin phosphorylation. Mutation of NF2/merlin rescued the myelin deficit in Rac1-CKO mice in vivo, and the shortened processes in cultured Rac1-CKO SCs in vitro. Mechanistically, cyclic adenosine monophosphate (cAMP) levels and E-cadherin expression were decreased in the absence of Rac1, and both were restored by mutation of NF2/merlin. Reduced cAMP is a cause of the myelin deficiency in Rac1-CKO mice, as elevation of cAMP by rolipram in Rac1-CKO mice in vivo allowed myelin formation. Thus NF2/merlin and cAMP function downstream of Rac1 signaling in SC myelination, and cAMP levels control Rac1-regulated SC myelination.

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“…Periaxin, a protein involved in peripheral nerve myelination was not expressed by these cells and additionally, IF analysis and transmission electron microscopy did not reveal neurites enwrapped by Schwann cell myelin sheaths. These results suggest that Schwann cells in our cultures were non-myelinating [55]. However, satellite cell processes were frequently observed to enclose neurites.…”

Section: Discussionmentioning

confidence: 87%

Primary Postnatal Dorsal Root Ganglion Culture from Conventionally Slaughtered Calves

et al. 2016

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Neurological disorders in ruminants have an important impact on veterinary health, but very few host-specific in vitro models have been established to study diseases affecting the nervous system. Here we describe a primary neuronal dorsal root ganglia (DRG) culture derived from calves after being conventionally slaughtered for food consumption. The study focuses on the in vitro characterization of bovine DRG cell populations by immunofluorescence analysis. The effects of various growth factors on neuron viability, neurite outgrowth and arborisation were evaluated by morphological analysis. Bovine DRG neurons are able to survive for more than 4 weeks in culture. GF supplementation is not required for neuronal survival and neurite outgrowth. However, exogenously added growth factors promote neurite outgrowth. DRG cultures from regularly slaughtered calves represent a promising and sustainable host specific model for the investigation of pain and neurological diseases in bovines.

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E‐cadherin expression in postnatal Schwann cells is regulated by the cAMP‐dependent protein kinase a pathway

Cited by 29 publications

References 39 publications

Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms

Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms

Rac1 Controls Schwann Cell Myelination through cAMP and NF2/merlin

Primary Postnatal Dorsal Root Ganglion Culture from Conventionally Slaughtered Calves

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