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Commitment of Satellite Cells Expressing the Calcium Channel α2δ1 Subunit to the Muscle Lineage

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Title: Commitment of Satellite Cells Expressing the Calcium Channel α2δ1 Subunit to the Muscle Lineage
Author(s): Tamayo, Tammy; Grajales, Liliana; Garcıa, Jesus
Abstract: Satellite cells can maintain or repair muscle because they possess stem cell properties, making them a valuable option for cell therapy. However, cell transplants into skeletal muscle of patients with muscular dystrophy are limited by donor cell attachment, migration, and survival in the host tissue. Cells used for therapy are selected based on specific markers present in the plasma membrane. Although many markers have been identified, there is a need to find a marker that is expressed at different states in satellite cells, activated, quiescent, or differentiated cell. Furthermore, the marker has to be present in human tissue. Recently we reported that the plasma membrane α2δ1 protein is involved in cell attachment and migration in myoblasts. The α2δ1 subunit forms a part of the L-type voltage-dependent calcium channel in adult skeletalmuscle.We found that the α2δ1 subunit is expressed in the majority of newly isolated satellite cells and that it appears earlier than the α1 subunits and at higher levels than the β or γ subunits.We also found that those cells that expressed α2δ1 would differentiate into muscle cells. This evidence indicates that the α2δ1 may be used as a marker of satellite cells that will differentiate into muscle.
Issue Date: 2012-11
Publisher: Hindawi Publishing Corporation
Citation Info: Tamayo T, Grajales L, Garcia J. Commitment of Satellite Cells Expressing the Calcium Channel alpha2delta1 Subunit to the Muscle Lineage. Journal of Signal Transduction. 2012;2012:460842. doi: 10.1155/2012/460842
Type: Article
Description: Copyright © 2012 Tammy Tamayo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ISSN: 2090-1747
Sponsor: National Heart, Lung and Blood Institute (T32 HL 07692).
Date Available in INDIGO: 2013-11-26

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