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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.