scholarly journals Raloxifene improves TNF‑α‑induced osteogenic differentiation inhibition of bone marrow mesenchymal stem cells and alleviates osteoporosis

2020 ◽  
Vol 20 (1) ◽  
pp. 309-314
Author(s):  
Fenghe Yang ◽  
Yusong Jia ◽  
Qi Sun ◽  
Chenying Zheng ◽  
Chuyin Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Tnf Α ◽  
Marrow Mesenchymal Stem Cells

Effects of Melatonin on Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in Inflammatory Environment by Regulating Mammalian Target of Rapamycin/Phosphatidylinositol 3-Kinase/Protein Kinase B Signaling

2021 ◽  
Vol 11 (4) ◽  
pp. 749-755
Author(s):  
Chi Zhang ◽  
Yuanhe Wang ◽  
Kang Sun ◽  
Dingzhu Yu ◽  
Shaoqi Tian
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Sod Activity ◽  
Alp Activity ◽  
Tnf Α ◽  
Marrow Mesenchymal Stem Cells

Human bone marrow mesenchymal stem cells (BMSCs) differentiation into special cell types is affected by inflammation. Melatonin has various effects such as anti-oxidation and immune regulation. However, melatonin’s effect on BMSCs osteogenic differentiation during inflammation has not been elucidated. Rat BMSCs were isolated and assigned into control group, inflammation group (1 μg/ml lipopolysaccharide, LPS) and melatonin group (100 μM melatonin was added to LPSstimulated BMSCs cells) followed by analysis of BMSCs proliferation by MTT assay, Caspase 3 and ALP activity, expression of Runx2 and OP by Real time PCR, ROS content and SOD activity, TNF-α and IL-1β secretion by ELISA and mTOR/PI3K/AKT signaling protein level by Western blot. LPS action on BMSCs significantly inhibits BMSCs proliferation, promotes Caspase 3 activity, inhibits ALP activity, decreases Runx2 and OP expression and SOD activity, increases ROS content and TNF-α and IL-1β secretion as well as reduced mTOR and p-PI3K level (P <0.05). Melatonin addition significantly reversed the above changes (P <0.05). Melatonin can regulate oxidative stress, inhibit inflammation, and promote BMSCs proliferation and osteogenic differentiation in inflammatory environment by activating mTOR/PI3K/AKT signaling pathway.

Bmi1 Induces Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Under Inflammatory Environment

2019 ◽  
Vol 9 (12) ◽  
pp. 1783-1789
Author(s):  
Chungang Dong ◽  
Junyu Wei
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Real Time Pcr ◽  
Alp Activity ◽  
Bmi1 Expression ◽  
Tnf Α ◽  
Marrow Mesenchymal Stem Cells

Bmi1 is a polycomb histone that regulates stem cells, but the role and mechanism of Bmi1 in bone marrow mesenchymal stem cells (BMSCs) differentiation has not been elucidated. Rat BMSCs were cultured in vitro and randomly divided into control group and inflammation group (treated with LPS). Bmi1 and Bmi1 siRNA were transfected into inflammatory BMSCs, followed by analysis of Bmi1 expression by Real time PCR, cell proliferation by MTT assay, Caspase3 activity, ALP activity, expression of Runx2, OP and PPARγ 2 by Real time PCR, as well as secretion of TNF-α and IL-1β by ELISA. In inflammatory environment, Bmi1 expression was significantly decreased, cell proliferation was significantly inhibited, along with increased Caspase3 activity, decreased ALP activity and the expression of Runx2 and OP, increased PPAR 2 expression and secretion of TNF-α and IL-1β (P < 0 05). Transfection of Bmi1 siRNA into inflammatory BMSCs further significantly aggravated the above changes (P < 0 05). Bmi1 plasmid transfected into inflammatory BMSCs significantly promoted Bmi1 expression and cell proliferation, decreased Caspase3 activity, increased ALP activity and expression of Runx2 and OP, decreased PPAR γ2 expression and TNF-α and IL-1β secretion (P < 0 05). Bmi1 expression is reduced in BMSCs under inflammation. Up-regulation of Bmi1 can inhibit the secretion of inflammatory factors, regulate the proliferation and apoptosis of BMSCs, and promote the proliferation and osteogenic differentiation of BMSCs.

Dextran-coated fluorapatite nanorods doped with lanthanides in labelling and directing osteogenic differentiation of bone marrow mesenchymal stem cells

2014 ◽  
Vol 2 (23) ◽  
pp. 3609-3617 ◽  
Author(s):  
Haifeng Zeng ◽  
Xiyu Li ◽  
Fang Xie ◽  
Li Teng ◽  
Haifeng Chen
Keyword(s):  
Tissue Engineering ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Tissue Engineering ◽  
Osteogenic Differentiation ◽  
Bone Tissue ◽  
Novel Approach ◽  
Marrow Mesenchymal Stem Cells

A novel approach for labelling and tracking BMSCs in bone tissue engineering by using dextran-coated fluorapatite nanorods doped with lanthanides.

miRNA-126 Inhibits Osteogenic Differentiation of Rat Bone Marrow Mesenchymal Stem Cells (BMSCs)

2022 ◽  
Vol 12 (4) ◽  
pp. 794-799
Author(s):  
Le Chang ◽  
Wei Duan ◽  
Chuang Wang ◽  
Jian Zhang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Mrna Level ◽  
Alizarin Red ◽  
Runx2 Expression ◽  
Alp Activity ◽  
Smad4 Protein ◽  
Marrow Mesenchymal Stem Cells

This study was to determine whether microRNA (miRNA)-126 regulates osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Rat BMSCs were extracted and stimulated for osteogenic differentiation. Functional experiments were conducted to assess miR-126’s impact on BMSCs differentiation. Western blot and RT-qPCR determined miR-126 expression. ALP activity detection and alizarin red staining detection were also performed. After osteogenic differentiation of BMSCs, miR-126 expression was gradually decreased over time. Overexpression of miR-26 decreased ALP activity, Notch signaling activity as well as declined Runx2 expression and calcium Salt nodules after treatment. Importantly, we found that Smad4 serves as a target of miR-126 while upregulation of the miRNA was accompanied with the decreased Smad4 protein expression without affecting the Smad4 mRNA level. In conclusion, miR-126 restrains osteogenic differentiation through inhibition of SMAD4 signaling, providing a novel insight into the mechanism.

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