Myotonic dystrophy CTG repeat expansion alters Ca2+channel functional expression in PC12 cells

Arturo Andrade, Mario Bermúdez de León, Oscar Hernández-Hernández, Bulmaro Cisneros, Ricardo Felix

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

We previously reported that expression of myotonic dystrophy (DM1) expanded CUG repeats impedes NGF-induced differentiation in a PC12 clone (CTG90 cells). Here, we present evidence for changes in the fractional contribution of distinct voltage-gated Ca2+channels, key elements in neurotrophin-promoted differentiation, to the total Ca2+current in the CTG90 cells. Patch-clamp recordings showed that the relative proportion of pharmacologically isolated Ca2+channel types differed between control and CTG90 cells. Particularly, the functional expression of N-type channels was significantly reduced. Though quantitative real-time RT-PCR revealed that transcripts for the pore-forming subunit encoding the N-type channels remained unchanged, the protein level analyzed by semi-quantitative Western blotting was down-regulated in the CTG90 cells. These data suggest modifications in the processing of N-type Ca2+channels in PC12 cells expressing the DM1 mutation. © 2007 Federation of European Biochemical Societies.
Original languageEnglish
Pages (from-to)4430-4438
Number of pages9
JournalFEBS Letters
DOIs
Publication statusPublished - 18 Sep 2007
Externally publishedYes

Fingerprint

Clone cells
Myotonic Dystrophy
PC12 Cells
Clamping devices
Nerve Growth Factors
Nerve Growth Factor
Cells
Electric potential
Processing
Proteins
Real-Time Polymerase Chain Reaction
Clone Cells
Western Blotting
Mutation

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Andrade, Arturo ; de León, Mario Bermúdez ; Hernández-Hernández, Oscar ; Cisneros, Bulmaro ; Felix, Ricardo. / Myotonic dystrophy CTG repeat expansion alters Ca2+channel functional expression in PC12 cells. In: FEBS Letters. 2007 ; pp. 4430-4438.
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abstract = "We previously reported that expression of myotonic dystrophy (DM1) expanded CUG repeats impedes NGF-induced differentiation in a PC12 clone (CTG90 cells). Here, we present evidence for changes in the fractional contribution of distinct voltage-gated Ca2+channels, key elements in neurotrophin-promoted differentiation, to the total Ca2+current in the CTG90 cells. Patch-clamp recordings showed that the relative proportion of pharmacologically isolated Ca2+channel types differed between control and CTG90 cells. Particularly, the functional expression of N-type channels was significantly reduced. Though quantitative real-time RT-PCR revealed that transcripts for the pore-forming subunit encoding the N-type channels remained unchanged, the protein level analyzed by semi-quantitative Western blotting was down-regulated in the CTG90 cells. These data suggest modifications in the processing of N-type Ca2+channels in PC12 cells expressing the DM1 mutation. {\circledC} 2007 Federation of European Biochemical Societies.",
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Myotonic dystrophy CTG repeat expansion alters Ca2+channel functional expression in PC12 cells. / Andrade, Arturo; de León, Mario Bermúdez; Hernández-Hernández, Oscar; Cisneros, Bulmaro; Felix, Ricardo.

In: FEBS Letters, 18.09.2007, p. 4430-4438.

Research output: Contribution to journalArticle

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AU - Andrade, Arturo

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AU - Cisneros, Bulmaro

AU - Felix, Ricardo

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