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. 2014 Jun 30;15(1):544. doi: 10.1186/1471-2164-15-544

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© Possidonio et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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A proposed model for the effects of MbCD-induced cholesterol depletion in chick myogenic cells. Our experiments suggest that cholesterol depletion by methyl-β-cyclodextrin (MbCD) enhances myoblast proliferation and its subsequent adhesion and fusion into multinucleated myotubes. Schematically, in normal myogenesis (A-C), myoblasts withdrawal from cell cycle (A) and became bipolar myoblasts. These bipolar myoblasts will then align with each other, guided by recognition between their plasma membranes (B) and fuse to form long multinucleated myotubes, with sharp striations and aligned nuclei (C). Conversely, myoblasts treated with MbCD (D) display an enhancement in cell proliferation (E) and fusion (F) leading to the formation of thicker myotubes (G). Note that nuclei (shown in blue) are well aligned at the periphery of control myotubes and are clustered in the central region of MbCD-treated myotubes. Areas of membrane adhesion are shown in red.