Modification of representational difference analysis applied to the isolation of forskolin‐regulated genes from Schwann cells

Bermingham, John R.; Shumas, Sue; Whisenhunt, Tom; Rosenfeld, Michael G.; Scherer, Steven S.

doi:10.1002/jnr.1046

Cited by 20 publications

(22 citation statements)

References 77 publications

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“…Interestingly, extracellular ATP failed to activate ERK1/2 in SCs grown without axons, which indicates that ectonucleotidases controlling the synthesis of adenosine from ATP might be more active in SCs cocultured with DRG axons. Consistent with this notion, agents that increase intracellular cAMP levels (and, thus, mimic axonal signals) have been shown recently to upregulate significantly an ATPase in SCs in culture (Bermingham et al, 2001).…”

Section: Adenosine Is An Activity-dependent Signal Activating Erk/mapmentioning

confidence: 59%

Adenosine: an activity-dependent axonal signal regulating MAP kinase and proliferation in developing Schwann cells

et al. 2004

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Nonsynaptic release of ATP from electrically stimulated dorsal root gangion (DRG) axons inhibits Schwann cell (SC) proliferation and arrests SC development at the premyelinating stage, but the specific types of purinergic receptor(s) and intracellular signaling pathways involved in this form of neuron-glia communication are not known. Recent research shows that adenosine is a neuron-glial transmitter between axons and myelinating glia of the CNS. The present study investigates the possibility that adenosine might have a similar function in communicating between axons and premyelinating SCs. Using a combination of pharmacological and molecular approaches, we found that mouse SCs in culture express functional adenosine receptors and ATP receptors, a far more complex array of purinergic receptors than thought previously. Adenosine, but not ATP, activates ERK/MAPK through stimulation of cAMP-linked A2 A adenosine receptors. Both ATP and adenosine inhibit proliferation of SCs induced by platelet-derived growth factor (PDGF), via mechanisms that are partly independent. In contrast to ATP, adenosine failed to inhibit the differentiation of SCs to the O4+ stage. This indicates that, in addition to ATP, adenosine is an activity-dependent signaling molecule between axons and premyelinating Schwann cells, but that electrical activity, acting through adenosine, has opposite effects on the differentiation of myelinating glia in the PNS and CNS.

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Section: Adenosine Is An Activity-dependent Signal Activating Erk/mapmentioning

confidence: 59%

Adenosine: an activity-dependent axonal signal regulating MAP kinase and proliferation in developing Schwann cells

et al. 2004

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“…Furthermore, elucidating whether the changes that we found are specific for the neuropathy caused by pmp22 overexpression or are general features of damaged sciatic nerves awaits comparison with other myelin mutant models. We have found many similarities in regulated processes with profiles generated from nerve response to injury or during SC maturation in development (as reported by Bermingham et al, 2001;Araki et al, 2001;Nagarajan et al, 2002;Schworer et al, 2003;Verheijen et al, 2003). However, the individual players involved in these processes may be different from those identified in our analysis.…”

Section: Discussionmentioning

confidence: 54%

“…involvement of particular molecular processes and components. Recent reports utilizing high-throughput techniques, such as differential display screenings and microarray analyses, have contributed to the unraveling of the complex mechanisms underlying the various aspects of myelin formation (Bermingham et al, 2001;Araki et al, 2001;Nagarajan et al, 2002;Schworer et al, 2003;Verheijen et al, 2003). These studies have led to the identification of known as well as novel molecules and events concerning the transition of SCs from proliferating toward myelinatation during nerve development, following nerve injury, and induced in vitro in SC cultures.…”

Section: Discussionmentioning

confidence: 98%

“…In recent years, attempts have been made to unravel the complex mechanisms underlying the various aspects of myelin formation by differential display screenings and microarray analyses (Bermingham et al, 2001;Araki et al, 2001;Nagarajan et al, 2002;Schworer et al, 2003;Verheijen et al, 2003). This has led to the identification of known as well as novel events concerning the transition of SCs from proliferating toward myelinating during nerve Supplementary Material for this article is available online at http:// www.mrw.interscience.wiley.com/suppmat/0360-4012/suppmat/ (www.…”

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confidence: 98%

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Expression profiling of sciatic nerve in a Charcot‐Marie‐Tooth disease type 1a mouse model

Asbroek

Verhamme

Groenigen

et al. 2005

J of Neuroscience Research

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Expression profiling was performed on sciatic nerve of normal mice and of transgenic mice overexpressing the peripheral myelin protein 22 kDa (PMP22). These mice represent a model for the hereditary peripheral neuropathy Charcot-Marie Tooth type 1A. Comparison of the profiles reveals that the proteasomal degradation pathway and various signaling mechanisms are up-regulated in the diseased nerve. The down-regulated processes represent cell shape and adhesion as well as cellular activity and metabolism. In addition, we found that the most significantly up-regulated differences could not be mapped on known transcripts and thus might represent not identified transcripts. Our data will be helpful to direct future research aimed at deciphering the molecular pathogenesis of the most prevalent hereditary peripheral neuropathy.

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“…To identify new molecules that are differentially expressed between the left and right sides of the embryo that participate in directing asymmetric morphogenesis, we used a modification of representation difference analysis (Bermingham et al, 2001;Hubank and Schatz, 1994). We isolated and sequenced 50 clones from each of the left-and right-enriched cDNA pools.…”

Section: Isolation Of the Chick Claudin-1 Cdna Clonementioning

confidence: 99%

Alterations in heart looping induced by overexpression of the tight junction protein Claudin-1 are dependent on its C-terminal cytoplasmic tail

Simard

Pietro

Young

et al. 2006

Mechanisms of Development

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In vertebrates, the positioning of the internal organs relative to the midline is asymmetric and evolutionarily conserved. A number of molecules have been shown to play critical roles in left-right patterning. Using representational difference analysis to identify genes that are differentially expressed on the left and right sides of the chick embryo, we cloned chick Claudin-1, an integral component of epithelial tight junctions. Here, we demonstrate that retroviral overexpression of Claudin-1, but not Claudin-3, on the right side of the chick embryo between HH stages 4 and 7 randomizes the direction of heart looping. This effect was not observed when Claudin-1 was overexpressed on the left side of the embryo. A small, but reproducible, induction of Nodal expression in the perinodal region on the right side of the embryo was noted in embryos that were injected with Claudin-1 retroviral particles on their right sides. However, no changes in Lefty, Pitx2 or cSnR expression were observed. In addition, Flectin expression remained higher in the left dorsal mesocardial folds of embryos with leftwardly looped hearts resulting from Claudin-1 overexpression on the right side of the embryo. We demonstrated that Claudin-1's C-terminal cytoplasmic tail is essential for this effect: mutation of a PKC phosphorylation site in the Claudin-1 C-terminal cytoplasmic domain at threonine-206 eliminates Claudin-1's ability to randomize the direction of heart looping. Taken together, our data provide evidence that appropriate expression of the tight junction protein Claudin-1 is required for normal heart looping and suggest that phosphorylation of its cytoplasmic tail is responsible for mediating this function. q

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Modification of representational difference analysis applied to the isolation of forskolin‐regulated genes from Schwann cells

Cited by 20 publications

References 77 publications

Adenosine: an activity-dependent axonal signal regulating MAP kinase and proliferation in developing Schwann cells

Adenosine: an activity-dependent axonal signal regulating MAP kinase and proliferation in developing Schwann cells

Expression profiling of sciatic nerve in a Charcot‐Marie‐Tooth disease type 1a mouse model

Alterations in heart looping induced by overexpression of the tight junction protein Claudin-1 are dependent on its C-terminal cytoplasmic tail

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