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

doi:10.1016/j.febslet.2007.08.020

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 journal › Article › peer-review

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 Ca ²⁺ channels, key elements in neurotrophin-promoted differentiation, to the total Ca ²⁺ current in the CTG90 cells. Patch-clamp recordings showed that the relative proportion of pharmacologically isolated Ca ²⁺ 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 Ca ²⁺ channels in PC12 cells expressing the DM1 mutation.

Original language	English
Pages (from-to)	4430-4438
Number of pages	9
Journal	FEBS Letters
Volume	581
Issue number	23
DOIs	https://doi.org/10.1016/j.febslet.2007.08.020
Publication status	Published - 18 Sept 2007
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by Grants from Conacyt to R.F., and from the Muscular Dystrophy Association (MDA-3693) to B.C. Doctoral and postdoctoral fellowships from Conacyt to A.A. and O.H.H, respectively, are gratefully acknowledged. We also thank Victor Tapia for assistance with cell cultures, and Dr. Manuel Hernandez (Cinvestav-IPN, Mexico) for his generous gift of the β-actin antibodies.

Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2007.08.020

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Cite this

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title = "Myotonic dystrophy CTG repeat expansion alters Ca2+channel functional expression in PC12 cells",

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 Ca 2+ channels, key elements in neurotrophin-promoted differentiation, to the total Ca 2+ current in the CTG90 cells. Patch-clamp recordings showed that the relative proportion of pharmacologically isolated Ca 2+ 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 Ca 2+ channels in PC12 cells expressing the DM1 mutation.",

author = "Arturo Andrade and {de Le{\'o}n}, {Mario Berm{\'u}dez} and Oscar Hern{\'a}ndez-Hern{\'a}ndez and Bulmaro Cisneros and Ricardo Felix",

note = "Funding Information: This work was supported by Grants from Conacyt to R.F., and from the Muscular Dystrophy Association (MDA-3693) to B.C. Doctoral and postdoctoral fellowships from Conacyt to A.A. and O.H.H, respectively, are gratefully acknowledged. We also thank Victor Tapia for assistance with cell cultures, and Dr. Manuel Hernandez (Cinvestav-IPN, Mexico) for his generous gift of the β-actin antibodies. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.",

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AU - Felix, Ricardo

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N2 - 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 Ca 2+ channels, key elements in neurotrophin-promoted differentiation, to the total Ca 2+ current in the CTG90 cells. Patch-clamp recordings showed that the relative proportion of pharmacologically isolated Ca 2+ 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 Ca 2+ channels in PC12 cells expressing the DM1 mutation.

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