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Background <p>MicroRNAs regulate the OPG/RANKL/RANK signaling pathway, which is crucial for postmenopausal osteoporosis (PMO) development. Explore the role of miR-217 in PMO by regulating the OPG/RANKL/RANK signaling pathway.</p> Methods <p>Taking osteoblast MC3T3-E1 as the research object, PMO model rats were further constructed. Reverse transcription quantitative PCR was used to detect the expression of miR-217 and related genes in cells and rat serum. Western blotting was used to detect the expression of relevant proteins. Enzyme-linked immunosorbent assay was used to detect the levels of related indicators in the serum of model rats.</p> Results <p>With the osteogenic differentiation of MC3T3-E1 cells, the relative expression level of miR-217 gradually decreases. Overexpression of miR-217 inhibits cell proliferation and osteogenic differentiation, while promoting cell apoptosis. Conversely, the knockdown of miR-217 elicited opposite outcomes. miR-217 was demonstrated to target OPG and thereby influence MC3T3 - E1 cells, with potential involvement of the OPG/RANKL/RANK signaling pathway. Additionally, the expression of miR-217 in the serum of rats with the PMO model was upregulated. Conversely, the inhibition of miR-217 demonstrated the capacity to augment bone metabolism and osteogenic differentiation in these model rats. Additionally, miR-217 was found to specifically target OPG. Knockdown of miR-217 upregulates OPG, inhibits RANKL-RANK interaction, and suppresses the NF-κB/MAPK pathways.</p> Conclusions <p>The expression of miR-217 is upregulated in PMO, and it may participate in the progression of the disease by regulating the OPG/RANKL/RANK signaling pathway.</p>

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MiR-217 participates in the progression of postmenopausal osteoporosis by regulating the OPG/RANKL/RANK pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月18日

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  • Xiaoxia Yang,
  • Qihua Jin,
  • Lihua Guo

摘要

Background

MicroRNAs regulate the OPG/RANKL/RANK signaling pathway, which is crucial for postmenopausal osteoporosis (PMO) development. Explore the role of miR-217 in PMO by regulating the OPG/RANKL/RANK signaling pathway.

Methods

Taking osteoblast MC3T3-E1 as the research object, PMO model rats were further constructed. Reverse transcription quantitative PCR was used to detect the expression of miR-217 and related genes in cells and rat serum. Western blotting was used to detect the expression of relevant proteins. Enzyme-linked immunosorbent assay was used to detect the levels of related indicators in the serum of model rats.

Results

With the osteogenic differentiation of MC3T3-E1 cells, the relative expression level of miR-217 gradually decreases. Overexpression of miR-217 inhibits cell proliferation and osteogenic differentiation, while promoting cell apoptosis. Conversely, the knockdown of miR-217 elicited opposite outcomes. miR-217 was demonstrated to target OPG and thereby influence MC3T3 - E1 cells, with potential involvement of the OPG/RANKL/RANK signaling pathway. Additionally, the expression of miR-217 in the serum of rats with the PMO model was upregulated. Conversely, the inhibition of miR-217 demonstrated the capacity to augment bone metabolism and osteogenic differentiation in these model rats. Additionally, miR-217 was found to specifically target OPG. Knockdown of miR-217 upregulates OPG, inhibits RANKL-RANK interaction, and suppresses the NF-κB/MAPK pathways.

Conclusions

The expression of miR-217 is upregulated in PMO, and it may participate in the progression of the disease by regulating the OPG/RANKL/RANK signaling pathway.