scholarly journals Mechanism of Action of Icariin in Bone Marrow Mesenchymal Stem Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Aofei Yang ◽  
Chaochao Yu ◽  
Qilin Lu ◽  
Hao Li ◽  
Zhanghua Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Mechanism Of Action ◽  
Underlying Mechanism ◽  
Bone Defects ◽  
Clinical Use ◽  
Regenerative Therapy ◽  
Herba Epimedii ◽  
Marrow Mesenchymal Stem Cells

Osteoporosis, femoral head necrosis, and congenital bone defects are orthopedic disorders characterized by reduced bone generation and insufficient bone mass. Bone regenerative therapy primarily relies on the bone marrow mesenchymal stem cells (BMSCs) and their ability to differentiate osteogenically. Icariin (ICA) is the active ingredient of Herba epimedii, a common herb used in traditional Chinese medicine (TCM) formulations, and can effectively enhance BMSC proliferation and osteogenesis. However, the underlying mechanism of ICA action in BMSCs is not completely clear. In this review, we provide an overview of the studies on the role and mechanism of action of ICA in BMSCs, to provide greater insights into its potential clinical use in bone regeneration.

scholarly journals Sinusoidal electromagnetic fields accelerate bone regeneration by boosting the multifunctionality of bone marrow mesenchymal stem cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Weigang Li ◽  
Wenbin Liu ◽  
Wei Wang ◽  
Jiachen Wang ◽  
Tian Ma ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Regeneration ◽  
Electromagnetic Fields ◽  
Bone Defects ◽  
Cell Scaffolds ◽  
Marrow Mesenchymal Stem Cells ◽  
Calvarial Defects

Abstract Background The repair of critical-sized bone defects is always a challenging problem. Electromagnetic fields (EMFs), used as a physiotherapy for bone defects, have been suspected to cause potential hazards to human health due to the long-term exposure. To optimize the application of EMF while avoiding its adverse effects, a combination of EMF and tissue engineering techniques is critical. Furthermore, a deeper understanding of the mechanism of action of EMF will lead to better applications in the future. Methods In this research, bone marrow mesenchymal stem cells (BMSCs) seeded on 3D-printed scaffolds were treated with sinusoidal EMFs in vitro. Then, 5.5 mm critical-sized calvarial defects were created in rats, and the cell scaffolds were implanted into the defects. In addition, the molecular and cellular mechanisms by which EMFs regulate BMSCs were explored with various approaches to gain deeper insight into the effects of EMFs. Results The cell scaffolds treated with EMF successfully accelerated the repair of critical-sized calvarial defects. Further studies revealed that EMF could not directly induce the differentiation of BMSCs but improved the sensitivity of BMSCs to BMP signals by upregulating the quantity of specific BMP (bone morphogenetic protein) receptors. Once these receptors receive BMP signals from the surrounding milieu, a cascade of reactions is initiated to promote osteogenic differentiation via the BMP/Smad signalling pathway. Moreover, the cytokines secreted by BMSCs treated with EMF can better facilitate angiogenesis and osteoimmunomodulation which play fundamental roles in bone regeneration. Conclusion In summary, EMF can promote the osteogenic potential of BMSCs and enhance the paracrine function of BMSCs to facilitate bone regeneration. These findings highlight the profound impact of EMF on tissue engineering and provide a new strategy for the clinical treatment of bone defects.

High glucose inhibits osteogenic differentiation of bone marrow mesenchymal stem cells via regulating miR-493-5p/ZEB2 signalling

2020 ◽  
Vol 167 (6) ◽  
pp. 613-621
Author(s):  
Zhongshu Zhai ◽  
Wanhong Chen ◽  
Qiaosheng Hu ◽  
Xin Wang ◽  
Qing Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
High Glucose ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
Downstream Target ◽  
Marrow Mesenchymal Stem Cells ◽  
Diabetic Osteoporosis

Abstract Diabetic osteoporosis (DOP) is attributed to the aberrant physiological function of bone marrow mesenchymal stem cells (BMSCs) under high glucose (HG) environment. MicroRNAs (miRNAs) are involved in the pathological processes of DOP. We aimed to explore the underlying mechanism of miRNA in DOP. BMSCs were cultured in osteogenic medium with HG to induce osteogenic differentiation, and the interaction between miR-493-5p and ZEB2 was assessed by luciferase assay. Herein, we found miR-493-5p is gradually reduced during osteogenic differentiation in BMSCs. HG treatment inhibits osteogenic differentiation and induces an up-regulation of miR-493-5p leading to reduced level of its downstream target ZEB2. Inhibition of miR-493-5p attenuates HG-induced osteogenic differentiation defects by upregulation of ZEB2. Mechanistically, miR-493-5p/ZEB2 signalling mediates HG-inhibited osteogenic differentiation by inactivation of Wnt/β-catenin signalling. More importantly, knockdown of miR-493-5p therapeutically alleviated the DOP condition in mice. HG prevents BMSCs osteogenic differentiation via up-regulation of miR-493-5p, which results in reduced level of ZEB2 by directly targeting its 3′-untranslated region of mRNA. Thus, miR-493-5p/ZEB2 is a potential therapeutic target and provides novel strategy for the treatment and management of DOP.

MicroRNA-21 Derived from Exosomes of Bone Marrow Mesenchymal Stem Cells (BMSCs) Alleviates Pancreatic Cancer by Downregulation of a Disintegrin and Metalloprotease 9 (ADAM9)

2021 ◽  
Vol 11 (12) ◽  
pp. 2346-2356
Author(s):  
Jie Zhong ◽  
Juncheng Tang ◽  
Kun Huang
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Specific Inhibitor ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
Marrow Mesenchymal Stem Cells ◽  
Novel Strategy

We aimed to explore underlying mechanism by which microRNA-21 (miR-21) derived from bone marrow mesenchymal stem cells (BMSCs) extracted exosomes (exo) in pancreatic cancer (PC). Bioinformatics analysis identified candidate miRNAs and target mRNAs in PC those were verified by luciferase reporter assay. BMSCs and exo were isolated and co-cultivated with PC cells. PC cells were then treated with plasmids loaded with miR-21 or a disintegrin and metalloprotease 9 (ADAM9), followed by detection of invasion, metastasis and apoptosis through Transwell assay and flow cytometry. MiR-21 was downregulated in PC tissues and cells, while ADAM9 was upregulated and positively correlated with poor prognosis. Overexpression of miR-21 restrained the capacities of proliferation, invasion and migration of PC cells by inhibiting ADAM9 expression. Specific inhibitor GW4869 reduced release of exo and declined miR-21 expression. Treatment with BMSC-exo containing miR-21 suppressed the malignant characteristics of cancer cells. MiR-21 derived from exo of BMSCs inhibited PC progression by ADAM9 down-regulation, providing insight into novel strategy against PC.

scholarly journals Wnt/β-catenin signaling mediates the abnormal osteogenic and adipogenic capabilities of bone marrow mesenchymal stem cells from chronic graft-versus-host disease patients

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Han-zhou Qi ◽  
Yi-ling Ye ◽  
Yuan Suo ◽  
Hong Qu ◽  
Hai-yan Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Graft Versus Host Disease ◽  
Underlying Mechanism ◽  
Hematopoietic Stem ◽  
Host Disease ◽  
Graft Versus Host ◽  
Ppar Γ ◽  
Marrow Mesenchymal Stem Cells

AbstractChronic graft-versus-host disease (cGVHD) is the main cause of non-relapse mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Mesenchymal stem cells (MSCs) in bone marrow (BM) remain unclear in the pathophysiology of cGVHD. In this study, we analyzed BM-MSCs from 66 patients after allo-HSCT, including 33 with active cGVHD and 33 without cGVHD. BM-MSCs showed similar morphology, frequency, phenotype, and proliferation in patients with or without cGVHD. MSCs from the active cGVHD group showed a decreased apoptosis rate (P < 0.01). Osteogenic capacity was increased while adipogenic capacity was decreased in the active cGVHD MSCs compared with no-cGVHD MSCs. The expressions of osteogenic gene RUNX2 and COL1A1 were higher (P < 0.001) while adipogenic gene PPAR-γ and FABP4 were lower (P < 0.001) in the active cGVHD MSCs than no-cGVHD MSCs. These changes were associated with the severity of cGVHD (P < 0.0001; r = 0.534, r = 0.476, r = −0.796, and r = −0.747, respectively in RUNX2, COL1A1, PPAR-γ, and FABP4). The expression of Wnt/β-catenin pathway ligand Wnt3a was increased in cGVHD-MSCs. The dysfunction of cGVHD-MSCs could be reversed by Dickkopf related protein 1(DKK1) to inhibit the binding of Wnt3a. In summary, the differentiation of BM-MSCs was abnormal in active cGVHD, and its underlying mechanism is the upregulated of Wnt3a through Wnt/β-catenin signaling pathway of MSCs.

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