Abstract
Notch signaling as a conserved cell fate regulator is involved in the regulation of cell quiescence, proliferation, differentiation and postnatal tissue regeneration. However, how Notch signaling regulates porcine satellite cells (PSCs) has not been elucidated. We stably transfected Notch1 intracellular domain (N1ICD) into PSCs to analyze the gene expression profile and miRNA-seq. The analysis of the gene expression profile identified 295 differentially-expressed genes (DEGs) in proliferating-N1ICD PSCs (P-N1ICD) and nine DEGs on differentiating-N1ICD PSCs (D-N1ICD), compared with that in control groups (P-Control and D-Control, respectively). Analyzing the underlying function of DEGs showed that most of the upregulated DEGs enriched in P-N1ICD PSCs are related to the cell cycle. Forty-four and 12 known differentially-expressed miRNAs (DEMs) were identified in the P-N1ICD PSCs and D-N1ICD PSCs group, respectively. Furthermore, we constructed the gene-miRNA network of the DEGs and DEMs. In P-N1ICD PSCs, miR-125a, miR-125b, miR-10a-5p, ssc-miR-214, miR-423 and miR-149 are downregulated hub miRNAs, whose corresponding hub genes are marker of proliferation Ki-67 (MKI67) and nuclear receptor binding SET domain protein 2 (WHSC1). By contrast, miR-27a, miR-146a-5p and miR-221-3p are upregulated hub miRNAs, whose hub genes are RUNX1 translocation partner 1 (RUNX1T1) and fibroblast growth factor 2 (FGF2). All the hub miRNAs and genes are associated with cell proliferation. Quantitative RT-PCR results are consistent with the gene expression profile and miRNA-seq results. The results of our study provide valuable information for understanding the molecular mechanisms underlying Notch signaling in PSCs and skeletal muscle development.
Highlights
Satellite cells as a primary source of muscle progenitors were initially identified in the frog skeletal muscle by Mauro in 1961 [1]
Notch1–3, HES1, HES2, HES5, HEY1 and hes related family bHLH transcription factor with YRPW motif-like (HEYL) were highly expressed in the quiescent satellite cells, which implies that Notch signaling is essential for maintenance of satellite cell quiescence
The expression of Notch signaling is decreased in the quiescent mice satellite cells with RBPJ defect, which facilitated the spontaneous activation of satellite cells and allowed them to undergo terminal differentiation, thereby resulting in a severe depletion of satellite cells’ pool [15,16]
Summary
Satellite cells as a primary source of muscle progenitors were initially identified in the frog skeletal muscle by Mauro in 1961 [1]. Activation of Notch signaling promotes proliferation in mice satellite cells [10,19,20]. There exist two waves of Notch signaling during the activation of satellite cells. The first wave of Notch signaling maintains the quiescent state of the satellite cells. The second wave of Notch signaling rises after satellite cells are activated [4]. This explanation is supported by Notch expression being decreased at first and increasing during muscle injury [9,16]. Notch signaling is related to satellite cell differentiation. How the Notch signaling pathway regulates skeletal muscle myogenesis is not clear
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