Literature DB >> 1724420

Expressing antisense P0 RNA in Schwann cells perturbs myelination.

G C Owens1, C J Boyd.   

Abstract

Primary Schwann cells were infected in vitro with a recombinant retrovirus expressing a dominant selectable marker, neomycin phosphotransferase (conferring resistance to the drug G418), and antisense P0 RNA under the control of the human beta-actin promoter. A proportion of the G418-resistant cells failed to form myelin when cocultured with dorsal root ganglion neurons under conditions that promote Schwann cell differentiation. These cells expressed high levels of P0 antisense RNA. Among the impaired cells, the majority had segregated and ensheathed individual axon but had not differentiated further. They did not express P0 but did express myelin- associated glycoprotein and galactocerebroside. A minority of partially inhibited Schwann cells were also observed that elaborated thin myelin sheaths containing variable numbers of compacted and noncompacted lamellae. These data indicate that restricting the level of P0 expression inhibits spiralling of the Schwann cell membrane and subsequent compaction.

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Year:  1991        PMID: 1724420     DOI: 10.1242/dev.112.2.639

Source DB:  PubMed          Journal:  Development        ISSN: 0950-1991            Impact factor:   6.868


  8 in total

1.  Developing Schwann cells acquire the ability to survive without axons by establishing an autocrine circuit involving insulin-like growth factor, neurotrophin-3, and platelet-derived growth factor-BB.

Authors:  C Meier; E Parmantier; A Brennan; R Mirsky; K R Jessen
Journal:  J Neurosci       Date:  1999-05-15       Impact factor: 6.167

Review 2.  Glycoproteins of myelin sheaths.

Authors:  R H Quarles
Journal:  J Mol Neurosci       Date:  1997-02       Impact factor: 3.444

3.  Transforming growth factor beta (TGFbeta) mediates Schwann cell death in vitro and in vivo: examination of c-Jun activation, interactions with survival signals, and the relationship of TGFbeta-mediated death to Schwann cell differentiation.

Authors:  D B Parkinson; Z Dong; H Bunting; J Whitfield; C Meier; H Marie; R Mirsky; K R Jessen
Journal:  J Neurosci       Date:  2001-11-01       Impact factor: 6.167

4.  Delivery of angiotensin II type 1 receptor antisense inhibits angiotensin action in neurons from hypertensive rat brain.

Authors:  D Lu; M K Raizada
Journal:  Proc Natl Acad Sci U S A       Date:  1995-03-28       Impact factor: 11.205

5.  Myelin protein zero gene mutated in Charcot-Marie-tooth type 1B patients.

Authors:  Y Su; D G Brooks; L Li; J Lepercq; J A Trofatter; J V Ravetch; R V Lebo
Journal:  Proc Natl Acad Sci U S A       Date:  1993-11-15       Impact factor: 11.205

6.  Retrovirus-mediated transfer of an angiotensin type I receptor (AT1-R) antisense sequence decreases AT1-Rs and angiotensin II action in astroglial and neuronal cells in primary cultures from the brain.

Authors:  D Lu; K Yu; M K Raizada
Journal:  Proc Natl Acad Sci U S A       Date:  1995-02-14       Impact factor: 11.205

7.  Retroviral-mediated gene transfer of the peripheral myelin protein PMP22 in Schwann cells: modulation of cell growth.

Authors:  G Zoidl; S Blass-Kampmann; D D'Urso; C Schmalenbach; H W Müller
Journal:  EMBO J       Date:  1995-03-15       Impact factor: 11.598

8.  Binding between the neural cell adhesion molecules axonin-1 and Nr-CAM/Bravo is involved in neuron-glia interaction.

Authors:  D M Suter; G E Pollerberg; A Buchstaller; R J Giger; W J Dreyer; P Sonderegger
Journal:  J Cell Biol       Date:  1995-11       Impact factor: 10.539

  8 in total

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