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LncRNA H19 contributes to Rh2-mediated MC3T3-E1cell proliferation by regulation of osteopontin
1Department of Orthopaedic Surgery, Heze MunicipalHospital; Heze, Shandong, 274031, China.
Abstract:
20(R)-ginsenoside Rh2 (Rh2) is one of the most active components of red ginseng, possessing the beneficial effects in cancer prevention and metabolic diseases. However, the detailed mechanisms that contribute to Rh2-mediated bone formation remain largely unknown. In this study, we assessed the expression of 17 long non-coding RNAs (lncRNAs) in cultured MC3T3-E1 cells under Rh2 treatments. We found that lncRNA H19 was significantly increased in Rh2-treated MC3T3-E1 cells. Expression of lncRNA H19 was promoted in a dose- and time-dependent manner after Rh2 treatments. Increased expression of lncRNA H19 resulted in osteopontin (OPN) overexpression in Rh2-treated MC3T3-E1 cells. Furthermore, knockdown of lncRNA H19 by specific siRNAs significantly abolished the Rh2-mediated cell proliferation effects. Knockdown of lncRNA H19 also decreased both mRNA and protein levels of OPN in the Rh2-treated cells, which was accomplished by inhibiting histones H3 and H4 acetylation of OPN promoter. Importantly, OPN knockdown fully blocked Rh2 induced MC3T3-E1 cell proliferation. Our results suggest that lncRNA H19 is an important contributor to Rh2-mediated MC3T3-E1 proliferation by regulation of OPN.
Insights
20(R)-ginsenoside Rh2 promotes MC3T3-E1 cell proliferation via long non-coding RNA H19. This mechanism involves upregulating osteopontin expression, highlighting H19
Area of Science:
- Molecular Biology
- Cell Biology
- Pharmacology
Background:
- 20(R)-ginsenoside Rh2 (Rh2) from red ginseng shows promise for cancer and metabolic diseases.
- The precise mechanisms of Rh2-induced bone formation are not fully understood.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cellular processes.
Purpose of the Study:
- To investigate the role of lncRNAs in Rh2-mediated osteoblast (MC3T3-E1) proliferation.
- To elucidate the molecular mechanisms underlying Rh2's effects on bone cells.
Main Methods:
- MC3T3-E1 cells were treated with Rh2, and lncRNA expression was analyzed.
- Quantitative real-time PCR and Western blotting were used to assess gene and protein expression.
- Small interfering RNAs (siRNAs) were employed to knock down lncRNA H19 and osteopontin (OPN).
- Histone acetylation of the OPN promoter was examined.
Main Results:
- Rh2 treatment significantly increased the expression of lncRNA H19 in MC3T3-E1 cells in a dose- and time-dependent manner.
- Increased lncRNA H19 expression correlated with osteopontin (OPN) overexpression.
- Knockdown of lncRNA H19 inhibited Rh2-induced cell proliferation and OPN levels.
- OPN knockdown completely abolished Rh2-mediated MC3T3-E1 cell proliferation.
- Rh2-induced OPN upregulation was linked to reduced histone acetylation of the OPN promoter.
Conclusions:
- lncRNA H19 is a key mediator of Rh2-induced MC3T3-E1 cell proliferation.
- The mechanism involves Rh2-induced upregulation of lncRNA H19, leading to OPN overexpression.
- This pathway highlights a novel mechanism for Rh2 in promoting bone formation.
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