miR-142a-5p promoted osteoblast differentiation via targeting nuclear factor IA.
Hairui YuanMengyue LiXue FengEndong ZhuBaoli WangPublished in: Journal of cellular physiology (2020)
miR-142a-5p plays critical roles in multiple biological processes and diseases, such as inflammation and tumorigenesis. However, it remains to be explored if and how miR-142a-5p contributes to osteoblast differentiation. In this study, our results showed that miR-142a-5p was highly expressed in bone tissue of mice and increased during osteogenesis in preosteoblast MC3T3-E1 cells. Supplementing miR-142a-5p activity using miR-142a-5p agomir promoted osteogenic differentiation in stromal cell line ST2 and preosteoblastic line MC3T3-E1. Conversely, miR-142a-5p antagomir, an inhibitor of endogenous miR-142a-5p, could reduce osteoblast differentiation in ST2 and MC3T3-E1 cells. Nuclear factor IA (NFIA), a site-specific transcriptional factor, was demonstrated to be directly targeted by miR-142a-5p. Overexpression of NFIA inhibited miR-142a-5p-mediated osteoblast differentiation in ST2 cells. Furthermore, mechanism explorations revealed that Wnt/β-catenin signaling transcriptionally regulated the expression of miR-142a-5p during osteogenic differentiation. β-catenin binds to the T-cell factor/lymphoid enhancer factor binding motif within the promoter of miR-142 and positively regulates its transcriptional activity. Our findings suggested that miR-142a-5p promoted osteoblast differentiation via targeting NFIA.
Keyphrases
- nuclear factor
- induced apoptosis
- transcription factor
- cell proliferation
- toll like receptor
- bone marrow
- cell cycle arrest
- bone regeneration
- gene expression
- stem cells
- oxidative stress
- dna methylation
- poor prognosis
- cancer therapy
- long non coding rna
- signaling pathway
- epithelial mesenchymal transition
- endoplasmic reticulum stress
- binding protein
- cell death
- drug delivery
- postmenopausal women
- dna binding
- pi k akt