Bone mesenchymal stem cell therapy for ovariectomized osteoporotic rats: a systematic review and meta-analysis

Jin, Zhenxiong; Chen, Jinman; Shu, Bing; Xiao, Yanhua; Tang, Dezhi

doi:10.1186/s12891-019-2851-2

Cited by 16 publications

(17 citation statements)

References 43 publications

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“…Our previous study demonstrated that osthole significantly stimulated osteoblast differentiation and bone formation by the activation of Wnt/β-catenin-Bmp2 signaling [ 24 ]. The previous meta-analysis showed that BMSCs promote bone cell maturation, ossification, and restore bone mechanical properties in osteoporotic fractures [ 25 ]. Although osthole can promote bone formation, its effect on bone resorption and the underlying mechanism is yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Osthole enhances the bone mass of senile osteoporosis and stimulates the expression of osteoprotegerin by activating β-catenin signaling

Jin

Liao

et al. 2021

Stem Cell Res Ther

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Introduction Osthole has a potential therapeutic application for anti-osteoporosis. The present study verified whether osthole downregulates osteoclastogenesis via targeting OPG. Methods In vivo, 12-month-old male mice were utilized to evaluate the effect of osthole on bone mass. In vitro, bone marrow stem cells (BMSCs) were isolated and extracted from 3-month-old OPG−/− mice and the littermates of OPG+/+ mice. Calvaria osteoblasts were extracted from 3-day-old C57BL/6J mice or 3-day-old OPG−/− mice and the littermates of OPG+/+ mice. Results Osthole significantly increased the gene and protein levels of OPG in primary BMSCs in a dose-dependent manner. The deletion of the OPG gene did not affect β-catenin expression. The deletion of the β-catenin gene inhibited OPG expression in BMSCs, indicating that osthole stimulates the expression of OPG via activation of β-catenin signaling. Conclusion Osthole attenuates osteoclast formation by stimulating the activation of β-catenin-OPG signaling and could be a potential drug for the senile osteoporosis.

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Section: Introductionmentioning

confidence: 99%

Osthole enhances the bone mass of senile osteoporosis and stimulates the expression of osteoprotegerin by activating β-catenin signaling

Jin

Liao

et al. 2021

Stem Cell Res Ther

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“…Osteoporosis can result in fractures and may increase economic cost and societal burden [3]. Previously, bone marrow mesenchymal stem cells (BMSCs) were administered as seed cells to improve BMD and used for tissue engineering [4]. However, the proliferation ability of BMSCs was limited, especially in older patients.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC00314 facilitates osteogenic differentiation of adipose-derived stem cells through the hsa-miR-129-5p/GRM5 axis via the Wnt signaling pathway

Zhang

Fan

et al. 2020

Stem Cell Res Ther

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Background: Many studies have shown that long noncoding RNAs (lncRNAs) are closely related to the stimulation of osteogenic differentiation of adipose-derived stem cells (ADSCs) and the prevention of osteoporosis. Current research aimed to investigate the novel lncRNA and explored the function and molecular mechanism of the LINC00314/miR-129-5p/GRM5 axis in regulating osteogenic differentiation of ADSCs. Methods: LncRNA and miRNA sequencing was performed in normal and osteogenic differentiation-induced ADSCs (osteogenic group). Abnormally expressed lncRNAs and miRNAs were obtained by the R software and the relative expression of LINC00314, miR-129-5p, and GRM5 during osteogenic induction was measured by RT-PCR. ADSCs were then transfected with pcDNA3.1-sh-LINC00314 and agomiR-129-5p. Alizarin red staining (ARS) and alkaline phosphatase (ALP) staining were performed to identify the mechanism of the LINC00314/miR-129-5p/GRM5 axis in regulating osteogenic differentiation of ADSCs. Results: LINC00314 was significantly upregulated in the group of osteogenic-induced ADSCs. LINC00314 and GRM5 mimics increased the early and late markers of osteogenic differentiation, which manifest in not only the markedly increased ALP activity but also higher calcium deposition, while miR-129-5p mimic had the opposite effects. LINC00314 directly targeted miR-129-5p through luciferase reporter assay, and miR-129-5p suppressed GRM5 expression. Moreover, the LINC00314/miR-129-5p/GRM5 regulatory axis activated the Wnt/β-catenin signaling pathway. Conclusions: LINC00314 confers contributory function in the osteogenic differentiation of ADSCs and thus the LINC00314/miR-129-5p/GRM5 axis may be a novel mechanism for osteogenic-related disease.

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“…Our previous study found that Osthole signi cantly stimulated osteoblast differentiation and bone formation by inducing the activation of Wnt/β-catenin-Bmp2 signaling [24] . And our previous metaanalysis of basic reports shows that BMSCs can promote bone call maturation, ossi cation and restore bone mechanical properties in osteoporotic fractures [25] . Although Osthole can promote bone formation, its effect on bone resorption and underlying mechanism remain unknown.…”

Section: Introductionmentioning

confidence: 96%

Osthole Inhibits Osteoclast Formation and Enhances Bone Mass of Bone Marrow Mesenchymal Stem cells by Activating β-catenin-OPG Signaling Pathway

Jin¹,

Liao²,

Da³

et al. 2020

Preprint

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Summary Osthole has potential therapeutic applications due to its antiosteoporotic. Our study suggested that osthole attenuates osteoclast formation by stimulating the activation of β-catenin-OPG signaling and could be a potential agent to inhibit bone resorption. Introduction Osthole has potential therapeutic applications due to its antiosteoporotic. we performed study to test if OPG is the target gene of osthole-attenuated osteoclastogenesis. Methods In vivo, using 12-month-old male mice to evaluate the effect of osthole on bone mass. In vitro, Bone marrow stem cells (BMSCs) were isolated, extracted from 3-month-old C57BL/6J mice, 3-month-old β-cateninfx/fx mice, or 3-month-old OPG−/− mice and its littermates of OPG+/+ mice. Results we found that osthole significantly increased the gene and protein levels of OPG expression in primary BMSCs dose-dependently. The deletion of the OPG gene did not affect β-catenin expression and the deletion of the β-catenin gene inhibited OPG expression in BMSCs, which indicated that osthole stimulated the expression of OPG through activation of β-catenin signaling. Conclusion Osthole attenuates osteoclast formation by stimulating the activation of β-catenin-OPG signaling and could be a potential agent to inhibit bone resorption.

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Bone mesenchymal stem cell therapy for ovariectomized osteoporotic rats: a systematic review and meta-analysis

Cited by 16 publications

References 43 publications

Osthole enhances the bone mass of senile osteoporosis and stimulates the expression of osteoprotegerin by activating β-catenin signaling

Osthole enhances the bone mass of senile osteoporosis and stimulates the expression of osteoprotegerin by activating β-catenin signaling

Long noncoding RNA LINC00314 facilitates osteogenic differentiation of adipose-derived stem cells through the hsa-miR-129-5p/GRM5 axis via the Wnt signaling pathway

Osthole Inhibits Osteoclast Formation and Enhances Bone Mass of Bone Marrow Mesenchymal Stem cells by Activating β-catenin-OPG Signaling Pathway

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