A potential regulatory network underlying distinct fate commitment of myogenic and adipogenic cells in skeletal muscle

23Citations
Citations of this article
18Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Mechanism controlling myo-adipogenic balance in skeletal muscle is of great significance for human skeletal muscle dysfunction and myopathies as well as livestock meat quality. In the present study, two cell subpopulations with particular potency of adipogenic or myogenic differentiation were isolated from neonatal porcine longissimus dorsi using the preplate method to detect mechanisms underlying distinct fate commitment of myogenic and adipogenic cells in skeletal muscle. Both cells share a common surface expression profile of CD29+ CD31- CD34- CD90+ CD105+, verifying their mesenchymal origin. A total of 448 differentially expressed genes (DEGs) (FDR < 0.05 and log 2 FC ≥ 1) between two distinct cells were identified via RNA-seq, including 358 up-regulated and 90 down-regulated genes in myogenic cells compared with adipogenic cells. The results of functional annotation and enrichment showed that 42 DEGs were implicated in cell differentiation, among them PDGFRα, ITGA3, ITGB6, MLCK and MLC acted as hubs between environment information processing and cellular process, indicating that the interaction of the two categories exerts an important role in distinct fate commitment of myogenic and adipogenic cells. Particularly, we are first to show that up-regulation of intracellular Ca 2+ -MLCK and Rho-DMPK, and subsequently elevated MLC, may contribute to the distinct commitment of myogenic and adipogenic lineages via mediating cytoskeleton dynamics.

Cite

CITATION STYLE

APA

Sun, W., He, T., Qin, C., Qiu, K., Zhang, X., Luo, Y., … Yin, J. (2017). A potential regulatory network underlying distinct fate commitment of myogenic and adipogenic cells in skeletal muscle. Scientific Reports, 7. https://doi.org/10.1038/srep44133

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free