Faculty Opinions recommendation of Interleukin-22 drives the proliferation, migration and osteogenic differentiation of mesenchymal stem cells: a novel cytokine that could contribute to new bone formation in spondyloarthropathies.

2018 ◽  
Author(s):  
Paul Emery ◽  
Leticia Garcia-Montoya
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Osteogenic Differentiation ◽  
New Bone Formation ◽  
Interleukin 22

scholarly journals Apoptosis Repressor with Caspase Domain (ARC) Promotes Bone Regeneration of Bone Marrow Derived Mesenchymal Stem Cells via Activating Fgf-2/PI3K/Akt Signaling

2020 ◽  
Author(s):  
Longwei Hu ◽  
Yang Wang ◽  
Hongya Pan ◽  
Kathreena Kadir ◽  
Jin Wen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Cell Apoptosis ◽  
Pcr Analysis ◽  
New Bone Formation

Abstract Objectives:This study aims to investigate whether ARC could promote survival and enhance osteogenic differentiation of bone marrow derived mesenchymal stem cells (BMSCs).Material and methods:Lentivirus transfection method was used to establish ARC overexpressed BMSCs. CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluoresence staining, ALP, ARS assay and RT-PCR analysis. Cells were seeded into CPC scaffolds, then inserted into subcutaneous of nude mice and the defect area of rat’s calvarium. Histological analysis was conducted to evaluate in vivo cell apoptosis and new bone formation ability of ARC overexpressed BMSCs. RNA-seq method was used to detect the possible mechanism of the effect of ARC on BMSCs. Results:ARC can promote BMSCs proliferation and inhibit its cell apoptosis. ARC can enhance BMSCs osteogenic differentiation in vitro. In vivo study revealed ARC can inhibit BMSCs’ apoptosis and increase its new bone formation ability. ARC regulates BMSCs mainly by activating Fgf-2/PI3K/Akt pathway.Conclusions: The present study suggested that ARC is a powerful agent to promote bone regeneration of BMSCs and provides a promising method for bone tissue engineering.

scholarly journals Apoptosis Repressor with Caspase Recruitment Domain (ARC) Promotes Bone Regeneration of Bone Marrow-Derived Mesenchymal Stem Cells by Activating Fgf-2/PI3K/Akt Signaling

2021 ◽  
Author(s):  
Longwei Hu ◽  
Yang Wang ◽  
Hongya Pan ◽  
Kathreena Kadir ◽  
Jin Wen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Cell Apoptosis ◽  
New Bone Formation ◽  
Caspase Recruitment Domain

Abstract Objectives: This study aims to investigate whether Apoptosis repressor with caspase recruitment domain (ARC) could promote survival and enhance osteogenic differentiation of bone marrow -derived mesenchymal stem cells (BMSCs). Materials and methods: The lentivirus transfection method was used to establish ARC -overexpressing BMSCs. The CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluorescence staining, ALP analysis, ARS assays and RT-PCR analysis. Cells were seeded into calcium phosphate cement (CPC) scaffolds and then inserted subcutaneously into nude mice and the defect area of the rat calvarium. Histological analysis was conducted to evaluate the in vivo cell apoptosis and new bone formation of the ARC -overexpressing BMSCs. RNA-seq was used to detect the possible mechanism of the effect of ARC on BMSCs. Results: ARC promoted BMSC proliferation and inhibited cell apoptosis. ARC enhanced BMSC osteogenic differentiation in vitro. An in vivo study revealed that ARC can inhibit BMSC apoptosis and increase new bone formation. ARC regulates BMSCs mainly by activating the Fgf-2/PI3K/Akt pathway. Conclusions: The present study suggests that A RC is a powerful agent for promoting bone regeneration of BMSCs and provides a promising method for bone tissue engineering.

scholarly journals Apoptosis repressor with caspase recruitment domain (ARC) promotes bone regeneration of bone marrow-derived mesenchymal stem cells by activating Fgf-2/PI3K/Akt signaling

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Longwei Hu ◽  
Yang Wang ◽  
Hongya Pan ◽  
Kathreena Kadir ◽  
Jin Wen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Cell Apoptosis ◽  
New Bone Formation ◽  
Caspase Recruitment Domain

Abstract Objectives This study aims to investigate whether apoptosis repressor with caspase recruitment domain (ARC) could promote survival and enhance osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs). Materials and methods The lentivirus transfection method was used to establish ARC-overexpressing BMSCs. The CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluorescence staining, ALP analysis, ARS assays, and RT-PCR analysis. Cells were seeded into calcium phosphate cement (CPC) scaffolds and then inserted subcutaneously into nude mice and the defect area of the rat calvarium. Histological analysis was conducted to evaluate the in vivo cell apoptosis and new bone formation of the ARC-overexpressing BMSCs. RNA-seq was used to detect the possible mechanism of the effect of ARC on BMSCs. Results ARC promoted BMSC proliferation and inhibited cell apoptosis. ARC enhanced BMSC osteogenic differentiation in vitro. An in vivo study revealed that ARC can inhibit BMSC apoptosis and increase new bone formation. ARC regulates BMSCs mainly by activating the Fgf-2/PI3K/Akt pathway. Conclusions The present study suggests that ARC is a powerful agent for promoting bone regeneration of BMSCs and provides a promising method for bone tissue engineering.

scholarly journals Apoptosis Repressor with Caspase Recruitment Domain (ARC) Promotes Bone Regeneration of Bone Marrow-Derived Mesenchymal Stem Cells by Activating Fgf-2/PI3K/Akt Signaling

2021 ◽  
Author(s):  
Longwei Hu ◽  
Yang Wang ◽  
Hongya Pan ◽  
Kathreena Kadir ◽  
Jin Wen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Cell Apoptosis ◽  
New Bone Formation ◽  
Caspase Recruitment Domain

Abstract Objectives: This study aims to investigate whether Apoptosis repressor with caspase recruitment domain (ARC) could promote survival and enhance osteogenic differentiation of bone marrow -derived mesenchymal stem cells (BMSCs). Materials and methods: The lentivirus transfection method was used to establish ARC -overexpressing BMSCs. The CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluorescence staining, ALP analysis, ARS assays and RT-PCR analysis. Cells were seeded into calcium phosphate cement (CPC) scaffolds and then inserted subcutaneously into nude mice and the defect area of the rat calvarium. Histological analysis was conducted to evaluate the in vivo cell apoptosis and new bone formation of the ARC -overexpressing BMSCs. RNA-seq was used to detect the possible mechanism of the effect of ARC on BMSCs. Results: ARC promoted BMSC proliferation and inhibited cell apoptosis. ARC enhanced BMSC osteogenic differentiation in vitro. An in vivo study revealed that ARC can inhibit BMSC apoptosis and increase new bone formation. ARC regulates BMSCs mainly by activating the Fgf-2/PI3K/Akt pathway. Conclusions: The present study suggests that A RC is a powerful agent for promoting bone regeneration of BMSCs and provides a promising method for bone tissue engineering.

scholarly journals Apoptosis Repressor with Caspase Recruitment Domain (ARC) Promotes Bone Regeneration of Bone Marrow-Derived Mesenchymal Stem Cells by Activating Fgf-2/PI3K/Akt Signaling

2021 ◽  
Author(s):  
Longwei Hu ◽  
Yang Wang ◽  
Hongya Pan ◽  
Kathreena Kadir ◽  
Jin Wen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Cell Apoptosis ◽  
New Bone Formation ◽  
Caspase Recruitment Domain

Abstract Objectives: This study aims to investigate whether Apoptosis repressor with caspase recruitment domain (ARC) could promote survival and enhance osteogenic differentiation of bone marrow -derived mesenchymal stem cells (BMSCs). Materials and methods: The lentivirus transfection method was used to establish ARC -overexpressing BMSCs. The CCK-8 method was used to detect cell proliferation. The BD Pharmingen™ APC Annexin V Apoptosis Detection kit was used to detect cell apoptosis. The osteogenic capacity was investigated by OCN immunofluorescence staining, ALP analysis, ARS assays and RT-PCR analysis. Cells were seeded into calcium phosphate cement (CPC) scaffolds and then inserted subcutaneously into nude mice and the defect area of the rat calvarium. Histological analysis was conducted to evaluate the in vivo cell apoptosis and new bone formation of the ARC -overexpressing BMSCs. RNA-seq was used to detect the possible mechanism of the effect of ARC on BMSCs. Results: ARC promoted BMSC proliferation and inhibited cell apoptosis. ARC enhanced BMSC osteogenic differentiation in vitro. An in vivo study revealed that ARC can inhibit BMSC apoptosis and increase new bone formation. ARC regulates BMSCs mainly by activating the Fgf-2/PI3K/Akt pathway. Conclusions: The present study suggests that A RC is a powerful agent for promoting bone regeneration of BMSCs and provides a promising method for bone tissue engineering.

scholarly journals Knockdown of POSTN Inhibits Osteogenic Differentiation of Mesenchymal Stem Cells From Patients With Steroid-Induced Osteonecrosis

2020 ◽  
Vol 8 ◽  
Author(s):  
Lizhi Han ◽  
Song Gong ◽  
Ruoyu Wang ◽  
Shaokai Liu ◽  
Bo Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Osteogenic Differentiation ◽  
Control Group ◽  
Nodule Formation ◽  
Matricellular Protein ◽  
Specific Gene ◽  
Endogenous Expression

Steroid-induced osteonecrosis of femoral head (SONFH) is a common and serious complication caused by long-term and/or excessive use of glucocorticoids (GCs). The decreased activity and abnormal differentiation of bone marrow mesenchymal stem cells (BMSCs) are considered to be one of the major reasons for the onset and progression of this disease. Periostin (POSTN) is a matricellular protein which plays an important role in regulating osteoblast function and bone formation. Sclerostin (SOST) is a secreted antagonist of Wnt signaling that is mainly expressed in osteocytes to inhibit bone formation. However, the exact role of POSTN and SOST in SONFH has not been reported yet. Therefore, we detected the differential expression of POSTN and SOST in BMSCs of SONFH Group patients, and Control Group was patients with traumatic ONFH (TONFH) and developmental dysplasia of the hip (DDH). Furthermore, we used lentiviral transfection to knockdown POSTN expression in BMSCs of patients with SONFH to study the effect of POSTN knockdown on the SOST expression and osteogenic differentiation of BMSCs. The results indicated that the endogenous expression of POSTN and SOST in BMSCs of SONFH Group was upregulated, compared with Control Group. POSTN was upregulated gradually while SOST was downregulated gradually at days 0, 3, and 7 of osteogenic differentiation of BMSCs in Control Group. Contrarily, POSTN was gradually downregulated while SOST was gradually upregulated during osteogenic differentiation of BMSCs in SONFH Group. This could be due to increased expression of SOST in BMSCs, which was caused by excessive GCs. In turn, the increased expression of POSTN in BMSCs may play a role in antagonizing the continuous rising of SOST during the osteogenic differentiation of BMSCs in patients with SONFH. POSTN knockdown significantly attenuated osteo-specific gene expression, alkaline phosphatase activity, and calcium nodule formation in vitro; thus inhibiting the osteogenic differentiation of BMSCs in patients with SONFH. Besides, POSTN knockdown upregulated SOST expression, increased GSK-3β activity, and downregulated β-catenin. These findings suggest that POSTN have an essential role in regulating the expression of SOST and osteogenic differentiation of BMSCs in patients with SONFH, and POSTN knockdown suppresses osteogenic differentiation by upregulating SOST and partially inactivating Wnt/β-catenin signaling pathway. Therefore, targeting POSTN and SOST may serve as a promising therapeutic target for the prevention and treatment of SONFH.

scholarly journals TNF-α-induced NF-κB activation upregulates microRNA-150-3p and inhibits osteogenesis of mesenchymal stem cells by targeting β-catenin

Open Biology ◽  
2016 ◽  
Vol 6 (3) ◽  
pp. 150258 ◽  
Author(s):  
Nan Wang ◽  
Zubin Zhou ◽  
Tianyi Wu ◽  
Wei Liu ◽  
Peipei Yin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Osteogenic Differentiation ◽  
Bone Cells ◽  
Bone Diseases ◽  
Cytokine Activation ◽  
Tnf Α ◽  
Marrow Mesenchymal Stem Cells ◽  
Underlying Mechanisms

Although systemic or local inflammation, commonly featured by cytokine activation, is implicated in patients with bone loss, the underlying mechanisms are still elusive. As microRNAs (miR), a class of small non-coding RNAs involved in essential physiological processes, have been found in bone cells, we aimed to investigate the role of miR for modulating osteogenesis in inflammatory milieu using human bone marrow mesenchymal stem cells (hBM-MSCs). Induced by proinflammatory cytokine TNF-α, miR-150-3p was identified as a key player in suppressing osteogenic differentiation through downregulating β-catenin, a transcriptional co-activator promoting bone formation. TNF-α treatment increased the levels of miR-150-3p, which directly targeted the 3′-UTR of β-catenin mRNA and in turn repressed its expression. In addition, we observed that miR-150-3p expression was increased by TNF-α via IKK-dependent NF-κB signalling. There are three putative NF-κB binding sites in the promoter region of miR-150, and we identified −686 region as the major NF-κB binding site for stimulation of miR-150 expression by TNF-α. Finally, the osteogenic differentiation of hBM-MSCs was inhibited by either miR-150-3p overexpression or TNF-α treatment, which was prevented by anti-miR-150-3p oligonucleotides. Taken together, our data suggested that miR-150-3p integrated inflammation signalling and osteogenic differentiation and may contribute to the inhibition effects of inflammation on bone formation, thus expanding the pathophysiological functions of microRNAs in bone diseases.

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