ArticleStem cell research & therapy2021
miR-133a silencing rescues glucocorticoid-induced bone loss by regulating the MAPK/ERK signaling pathway.
Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- The characteristic expression of circulatingFrontiers in endocrinology · 2024Pooled it
- MicroRNAs in osteoporosis: current evidence and clinical perspectives.Reumatologia · 2026Review
- GLP-2-carrying exosomes alleviate osteoporosis by upregulating miR-378a-3p to inhibit osteoclastic differentiation and NF-κB-MAPK pathway.Journal of orthopaedic surgery and research · 2025Article
- microRNA-576-5p ameliorates dexamethasone-induced BMSC injury by suppressing ANXA2.Scientific reports · 2025Article
- Identification of lactylation-related biomarkers in osteoporosis from transcriptome and single-cell data.Frontiers in endocrinology · 2025Article
- Jintiange capsule ameliorates glucocorticoid-induced osteonecrosis of the femoral head in rats by regulating the activity and differentiation of BMSCs.Journal of traditional and complementary medicine · 2024Article
- Application of dental pulp stem cells for bone regeneration.Frontiers in medicine · 2024Review
- Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.Frontiers in cell and developmental biology · 2024Review
- Integrated analysis of muscle transcriptome, miRNA, and proteome of Chinese indigenous breed Ningxiang pig in three developmental stages.Frontiers in genetics · 2024Article
- Regulation of idiopathic pulmonary fibrosis: a cross-talk between TGF-Frontiers in medicine · 2024Review
- Association between dietary selenium intake and the prevalence of osteoporosis and its role in the treatment of glucocorticoid-induced osteoporosis.Journal of orthopaedic surgery and research · 2023Article
- Glucocorticoid-induced activation of NOX/ROS/NF-κB signaling in MSCs contributes to the development of GONFH.Apoptosis : an international journal on programmed cell death · 2023Article
- Pathogenic mechanisms of glucocorticoid-induced osteoporosis.Cytokine & growth factor reviews · 2023Review
- Update on the Role of Glucocorticoid Signaling in Osteoblasts and Bone Marrow Adipocytes During Aging.Current osteoporosis reports · 2023Review
- Immune-related geneFrontiers in genetics · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDysfunction of mesenchymal stem cells (MSCs) is recognized as critical to the pathogenesis of glucocorticoid-induced osteoporosis (GIO), suggesting the potential of MSC-targeting interventions for this disorder. As the miR-133a has been shown to play an important role in bone metabolism, we hypothesized that miR-133a may also be involved in GIO.
methodsIn the in vitro study, we examined the effect of miR-133a antagomir on DEX-treated MSCs, including proliferation, apoptosis, osteoblast, and adipocyte differentiation, then, we explored the mechanism of these effects of miR-133a silencing through measuring the phosphorylation of ERK1/2 and its regulator FGFR1 via western blot and qRT-PCR. In the in vivo study, we developed a GIO rat model by injecting methylprednisolone and modulated the miR-133a expression in the femur by intramedullary injection of the miR-133a antagomir, and then micro-CT analyses and histological staining of the femurs were used to investigate the effect of miR-133a silencing on bone loss of the GIO rats.
resultsqRT-PCR analysis indicated that glucocorticoid induced high miR-133a expression in MSCs and animal models. The in vitro study showed that miR-133a antagomir significantly promoted cell proliferation, viability, and osteoblast differentiation and inhibited adipocyte differentiation in DEX-treated MSCs. Furthermore, the expression of p-ERK1/2 and FGFR1 in DEX-treated MSCs was also upregulated by miR-133a antagomir. Then we investigated the effect of miR-133a silencing on the bone architecture of GIO models, micro-CT analysis showed that miR-133a antagomir attenuated the loss of bone mass and improved the trabecular and cortical parameters induced by methylprednisolone. Histological study showed that miR-133a silencing simultaneously increased bone formation and decreased marrow fat accumulation in GIO rats.
conclusionsOur findings suggested that miR-133a is strongly associated with GIO and similar disorders induced by glucocorticoids in MSCs. Silencing miR-133a resulted in positive effects on GC-treated MSCs and on bone loss in GIO animal models. Moreover, the FGFR1-MAPK/ERK signaling may be involved in the protective effect of miR-133a silencing.
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