The Open Infectious Diseases Journal
2009, 3 : 21-26Published online 2009 January 21. DOI: 10.2174/1874279300903010021
Publisher ID: TOIDJ-3-21
RESEARCH ARTICLE
Antimyogenic Effect of SARS-CoV Spike Protein in C2C12 Myoblasts
2 Current Address: Waseda-Olympus Bioscience Research Institute, 11 Biopolis Way, Helios # 05-01/02, 138667, Singapore
3 Current Address: Pharmaceutical Services Corporation, 26 Boonlay Way, #01-92 TradeHub 21, 609970, Singapore
* Address correspondence to this author at the Waseda-Olympus Bioscience Research Institute, 11 Biopolis Way, Helios #05-01/02, 138667, Singapore. E-mail: chouchihfong@yahoo.com
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.