Osteogenic differentiation potential of human bone marrow‐derived mesenchymal stem cells enhanced by <scp>bacoside‐A</scp>

Ramesh, Thiyagarajan

doi:10.1002/cbf.3596

Cited by 11 publications

(5 citation statements)

References 63 publications

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“…Stem cell therapy is developing rapidly and has been used to treat various diseases, including bone-related diseases. 25 As the common progenitor of adipocytes and osteoblasts, hBMSCs need to be maintained in a delicate balance of commitment. 26 hBMSCs also play an important role in peri-implantitis.…”

Section: Discussionmentioning

confidence: 99%

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis

et al. 2022

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Objective Peri-implantitis is characterized by peri-implant mucositis and alveolar bone resorption. This study investigated cholecystokinin ( CCK) expression and the mechanism underlying its involvement in peri-implantitis. Methods mRNA sequencing was performed using the Gene Expression Omnibus database GSE106090. Human bone marrow mesenchymal stem cells (hBMSCs) were pretreated with various concentrations of CCK (0, 10, 30, or 100 nM) for 1 hour before induction in osteogenic differentiation medium for 2 weeks. Alkaline phosphatase (ALP) activity was determined, and the cells were stained with alizarin red. The expression levels of TNFα and the osteogenic markers ALP, RUNX2, and OCN were measured using quantitative real-time PCR. TNFα, phosphorylated P65, and total P65 levels were determined by western blot. Results Compared with healthy individuals, 262 and 215 genes were up- and down-regulated, respectively, in the periodontal tissues of patients with peri-implantitis. CCK expression was significantly upregulated in patients with peri-implantitis. CCK reduced ALP activity, osteogenic differentiation, and levels of the osteogenic markers ALP, RUNX2, and OCN. Moreover, CCK promoted levels of TNFα and phosphorylated P65, which is a marker of activation for the NF-κB inflammatory pathway. Conclusions CCK regulates osteogenic differentiation through the TNFα/NF-κB axis in peri-implantitis.

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Section: Discussionmentioning

confidence: 99%

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis

et al. 2022

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“…Bone marrow mesenchymal stem cells (BMSCs) are progenitor cells that are capable of self-renewal and have the potential for multidirectional differentiation such as adipogenesis, osteogenesis, and chondrogenesis [ 4 , 5 ]. Importantly, promoting osteogenic differentiation of BMSCs is currently a hot topic in the treatment of osteoporosis [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

mir-150-5p inhibits the osteogenic differentiation of bone marrow-derived mesenchymal stem cells by targeting irisin to regulate the p38/MAPK signaling pathway

Qi,

Zhang,

Dong

et al. 2024

J Orthop Surg Res

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Purpose To study the effect of miR-150-5p on the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs), and further explore the relationship between its regulatory mechanism and irisin. Methods We isolated mouse BMSCs, and induced osteogenic differentiation by osteogenic induction medium. Using qPCR to detect the expression of osteogenic differentiation-related genes, western blot to detect the expression of osteogenic differentiation-related proteins, and luciferase reporter system to verify that FNDC5 is the target of miR-150-5p. Irisin intraperitoneal injection to treat osteoporosis in mice constructed by subcutaneous injection of dexamethasone. Results Up-regulation of miR-150-5p inhibited the proliferation of BMSCs, and decreased the content of osteocalcin, ALP activity, calcium deposition, the expression of osteogenic differentiation genes (Runx2, OSX, OCN, OPN, ALP and BMP2) and protein (BMP2, OCN, and Runx2). And down-regulation of miR-150-5p plays the opposite role of up-regulation of miR-150-5p on osteogenic differentiation of BMSCs. Results of luciferase reporter gene assay showed that FNDC5 gene was the target gene of miR-150-5p, and miR-150-5p inhibited the expression of FNDC5 in mouse BMSCs. The expression of osteogenic differentiation genes and protein, the content of osteocalcin, ALP activity and calcium deposition in BMSCs co-overexpressed by miR-150-5p and FNDC5 was significantly higher than that of miR-150-5p overexpressed alone. In addition, the overexpression of FNDC5 reversed the blocked of p38/MAPK pathway by the overexpression of miR-150-5p in BMSCs. Irisin, a protein encoded by FNDC5 gene, improved symptoms in osteoporosis mice through intraperitoneal injection, while the inhibitor of p38/MAPK pathway weakened this function of irisin. Conclusion miR-150-5p inhibits the osteogenic differentiation of BMSCs by targeting irisin to regulate the/p38/MAPK signaling pathway, and miR-150-5p/irisin/p38 pathway is a potential target for treating osteoporosis.

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“…Bone marrow-derived MSCs (BMSCs) are the most widely used stem cells in cell therapy and tissue engineering owing to their properties in anti-inflammation, angiogenesis, organ repair, and bone regeneration [3][4][5][6]. Under the damage to osseous tissues, BMSCs can be differentiated into bone-forming osteoblasts to repair bone defects [7,8]. Moreover, compared with other types of MSCs, such as adipose tissue MSCs, BMSCs show a superior potential for osteogenic differentiation (OD) in vitro as evidenced by more mineralized nodules, stronger alkaline phosphatase (ALP) activity, and higher levels of osteogenic specific genes [9].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanism of Long Noncoding RNA SNHG14 in Osteogenic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells through the NEDD4L/FOXA2/PCP4 Axis

Wang

Fan

et al. 2023

Stem Cells International

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Bone marrow-derived mesenchymal stem cells (BMSCs) have a superior potential of osteogenic differentiation (OD) and a promising stem cell type to treat bone defects. This study sought to investigate the molecular mechanism of long noncoding RNA small nucleolar RNA host gene 14 (SNHG14) in OD of BMSCs. Western blot analysis or RT-qPCR showed that SNHG14, neural precursor cell expressed developmentally downregulated 4-like (NEDD4L), and Purkinje cell protein 4 (PCP4) were upregulated whereas forkhead box A2 (FOXA2) was declined in OD of BMSCs. RT-qPCR and cell staining showed that SNHG14 downregulation repressed OD of BMSCs, as manifested by reductions in osteopontin and osteocalcin levels, the mineralization degree, and alkaline phosphatase activity. RNA/Co/chromatin immunoprecipitation and dual-luciferase assays and determination of mRNA stability and ubiquitination level showed that SNHG14 bound to human antigen R improves NEDD4L mRNA stability and expression, further promoted FOXA2 ubiquitination to inhibit FOXA2 expression, and then reduced FOXA2 enrichment on the PCP4 promoter to upregulate PCP4 transcription. Functional rescue experiments showed that the overexpression of NEDD4L or PCP4 and knockdown of FOXA2 both attenuated the inhibition of SNHG14 downregulation on OD of BMSCs. Overall, our findings suggested that SNHG14 promoted OD of BMSCs through the NEDD4L/FOXA2/PCP4 axis.

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Osteogenic differentiation potential of human bone marrow‐derived mesenchymal stem cells enhanced by bacoside‐A

Cited by 11 publications

References 63 publications

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis

CCK regulates osteogenic differentiation through TNFα/NF-κB in peri-implantitis

mir-150-5p inhibits the osteogenic differentiation of bone marrow-derived mesenchymal stem cells by targeting irisin to regulate the p38/MAPK signaling pathway

Molecular Mechanism of Long Noncoding RNA SNHG14 in Osteogenic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells through the NEDD4L/FOXA2/PCP4 Axis

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