RESEARCH ARTICLE
Antimyogenic Effect of SARS-CoV Spike Protein in C2C12 Myoblasts
Chih-Fong Chou1, 2, *, Geetha Mahadevappa1, 3, Wanjin Hong1, Yee-Joo Tan1
Article Information
Identifiers and Pagination:
Year: 2009Volume: 3
First Page: 21
Last Page: 26
Publisher Id: TOIDJ-3-21
DOI: 10.2174/1874279300903010021
Article History:
Received Date: 18/11/2007Revision Received Date: 17/12/2008
Acceptance Date: 23/12/2008
Electronic publication date: 21/1/2009
Collection year: 2009
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
C2C12 myoblasts serve as well-established model system to study myogenesis, as they fuse to form multinucleated myotubes. Severe acute respiratory syndrome coronavirus (SARS–CoV) spike (S) protein plays a crucial role in viral entry. Exogenous expression of S protein in C2C12 myoblasts inhibits the formation of myotubes. Global changes in gene expression were studied in C2C12 cells expressing S protein using oligonucleotide microarray analysis. The expression profile showed that, most of the myogenic marker genes were downregulated. Next, we used RT-PCR analysis to reexamine some downregulated and upregulated genes. To further study the antimyogenic effects induced by the S protein, we introduced antisense Plf (proliferin), an upregulated gene, into the antimyogenic cells. Antisense Ace2 (angiotensin-converting enzyme 2), the cellular receptor of S protein, was also introduced into C2C12 myoblasts. Results indicated that antimyogenic effect induced by S protein was partially rescued in cells expressing antisense Plf, while C2C12 cells expressing antisense Ace2 showed upregulation of Plf.