scholarly journals Synergistic Effects of Orbital Shear Stress onIn VitroGrowth and Osteogenic Differentiation of Human Alveolar Bone-Derived Mesenchymal Stem Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-18 ◽  
Author(s):  
Ki Taek Lim ◽  
Jin Hexiu ◽  
Jangho Kim ◽  
Hoon Seonwoo ◽  
Pill-Hoon Choung ◽  
...  
Keyword(s):  
Stem Cells ◽  
Shear Stress ◽  
Mesenchymal Stem Cells ◽  
Alveolar Bone ◽  
Synergistic Effects ◽  
Osteoblastic Differentiation ◽  
Bone Morphogenetic Protein 2 ◽  
Control Group ◽  
Protein Levels ◽  
Morphogenetic Protein

Cellular behavior is dependent on a variety of physical cues required for normal tissue function. In order to mimic native tissue environments, human alveolar bone-derived mesenchymal stem cells (hABMSCs) were exposed to orbital shear stress (OSS) in a low-speed orbital shaker. The synergistic effects of OSS on proliferation and differentiation of hABMSCs were investigated. In particular, we induced the osteoblastic differentiation of hABMSCs cultured in the absence of OM by exposing hABMSCs to OSS (0.86–1.51 dyne/cm2). Activation of Cx43 was associated with exposure of hABMSCs to OSS. The viability of cells stimulated for 10, 30, 60, 120, and 180 min/day increased by approximately 10% compared with that of control. The OSS groups with stimulation of 10, 30, and 60 min/day had more intense mineralized nodules compared with the control group. In quantification of vascular endothelial growth factor (VEGF) and bone morphogenetic protein-2 (BMP-2) protein, VEGF protein levels under stimulation for 10, 60, and 180 min/day and BMP-2 levels under stimulation for 60, 120, and 180 min/day were significantly different compared with those of the control. In conclusion, the results indicated that exposing hABMSCs to OSS enhanced their differentiation and maturation.

scholarly journals A NOTCH1/LSD1/BMP2 co-regulatory network mediated by miR-137 negatively regulates osteogenesis of human adipose-derived stem cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Cong Fan ◽  
Xiaohan Ma ◽  
Yuejun Wang ◽  
Longwei Lv ◽  
Yuan Zhu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Osteoblastic Differentiation ◽  
Negative Control ◽  
Bone Morphogenetic Protein 2 ◽  
Luciferase Reporter ◽  
Adipose Derived Stem Cells ◽  
Differentiation Potential ◽  
Lineage Differentiation ◽  
Morphogenetic Protein ◽  
Genes Expression

Abstract Background MicroRNAs have been recognized as critical regulators for the osteoblastic lineage differentiation of human adipose-derived stem cells (hASCs). Previously, we have displayed that silencing of miR-137 enhances the osteoblastic differentiation potential of hASCs partly through the coordination of lysine-specific histone demethylase 1 (LSD1), bone morphogenetic protein 2 (BMP2), and mothers against decapentaplegic homolog 4 (SMAD4). However, still numerous molecules involved in the osteogenic regulation of miR-137 remain unknown. This study aimed to further elucidate the epigenetic mechanisms of miR-137 on the osteogenic differentiation of hASCs. Methods Dual-luciferase reporter assay was performed to validate the binding to the 3′ untranslated region (3′ UTR) of NOTCH1 by miR-137. To further identify the role of NOTCH1 in miR-137-modulated osteogenesis, tangeretin (an inhibitor of NOTCH1) was applied to treat hASCs which were transfected with miR-137 knockdown lentiviruses, then together with negative control (NC), miR-137 overexpression and miR-137 knockdown groups, the osteogenic capacity and possible downstream signals were examined. Interrelationships between signaling pathways of NOTCH1-hairy and enhancer of split 1 (HES1), LSD1 and BMP2-SMADs were thoroughly investigated with separate knockdown of NOTCH1, LSD1, BMP2, and HES1. Results We confirmed that miR-137 directly targeted the 3′ UTR of NOTCH1 while positively regulated HES1. Tangeretin reversed the effects of miR-137 knockdown on osteogenic promotion and downstream genes expression. After knocking down NOTCH1 or BMP2 individually, we found that these two signals formed a positive feedback loop as well as activated LSD1 and HES1. In addition, LSD1 knockdown induced NOTCH1 expression while suppressed HES1. Conclusions Collectively, we proposed a NOTCH1/LSD1/BMP2 co-regulatory signaling network to elucidate the modulation of miR-137 on the osteoblastic differentiation of hASCs, thus providing mechanism-based rationale for miRNA-targeted therapy of bone defect.

scholarly journals Bone remodeling using a three-dimensional chitosan - hydroxyapatite scaffold seeded with hypoxic conditioned human amnion mesenchymal stem cells

2021 ◽  
Vol 54 (2) ◽  
pp. 68
Author(s):  
Michael Josef Kridanto Kamadjaja
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Remodeling ◽  
Three Dimensional ◽  
Wistar Rat ◽  
Control Group ◽  
Human Amnion ◽  
Morphogenetic Protein ◽  
Hydroxyapatite Scaffold ◽  
Endothelial Growth Factor

Background: Bone regeneration studies involving the use of chitosan–hydroxyapatite (Ch-HA) scaffold seeded with human amnion mesenchymal stem cells (hAMSCs) have largely incorporated tissue engineering experiments. However, at the time of writing, the results of such investigations remain unclear. Purpose: The aim of this study was to determine the osteogenic differentiation of the scaffold Ch-HA that is seeded with hAMSCs in the regeneration of calvaria bone defect. Methods: Ch-HA scaffold of 5 mm diameter and 2 mm height was created by lyophilisation and desalination method. hAMSCs were cultured in hypoxia environment (5% oxygen, 10% carbon dioxide, 15% nitrogen) and seeded on the scaffold. Twenty male Wistar rat subjects (8 – 10 weeks, 200 - 250 grams) were randomly divided into two groups: control and hydroxyapatite scaffold (HAS). Defects (similar size to scaffold size) were created in the calvaria bone of the all-group subjects, but a scaffold was subsequently implanted only in the treatment group members. Control group left without treatment. After observation lasting 1 and 8 weeks, the subjects were examined histologically and immunohistochemically. Statistical analysis was done using ANOVA test. Results: Angiogenesis; expression of vascular endothelial growth factor; bone morphogenetic protein; RunX-2; alkaline phosphatase; type-1 collagen; osteocalcin and the area of new trabecular bone were all significantly greater in the HAS group compared to the control group. Conclusion: The three-dimensional Ch-HA scaffold seeded with hypoxic hAMSCs induced bone remodeling in calvaria defect according to the expression of the osteogenic and angiogenic marker.

Murine spinal fusion induced by engineered mesenchymal stem cells that conditionally express bone morphogenetic protein—2

2005 ◽  
Vol 3 (1) ◽  
pp. 47-52 ◽  
Author(s):  
Amir Hasharoni ◽  
Yoram Zilberman ◽  
Gadi Turgeman ◽  
Gregory A. Helm ◽  
Meir Liebergall ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Spinal Fusion ◽  
Genetically Engineered ◽  
Bone Morphogenetic Protein 2 ◽  
Content Type ◽  
Histological Studies ◽  
Morphogenetic Protein ◽  
Fine Print

Object. The authors hypothesized that spinal fusion can be achieved and monitored by using cell-mediated gene therapy. Mesenchymal stem cells (MSCs) genetically engineered to express recombinant human bone morphogenetic protein—2 (rhBMP-2) conditionally, were implanted into the paraspinal muscles of mice to establish spinal fusion. The goal was to demonstrate an MSC-based gene therapy platform in which controlled gene expression is used to obtain spinal fusion in a murine model. Methods. Mesenchymal stem cells expressing the rhBMP-2 gene were injected into the paravertebral muscle in mice. Bone formation in the paraspinal region was longitudinally followed by performing micro—computerized tomography scanning, histological studies, and an analysis of osteocalcin expression to demonstrate the presence of engrafted engineered MSCs. The minimal period of rhBMP-2 expression by the engineered MSCs required to induce fusion was determined. The results of this study demonstrate that genetically engineered MSCs induce bone formation in areas adjacent to and touching the posterior elements of the spine. This newly formed bone fuses the spine, as demonstrated by radiological and histological studies. The authors demonstrate that injected cells induce active osteogenesis at the site of implantation for up to 4 weeks postinjection. They found that a 7-day induction of rhBMP-2 expression in genetically engineered MSCs was sufficient to form new bone tissue, although the quantity of this bone increased as longer expression periods were implemented. Conclusions. After their injection genetically engineered MSCs can efficiently form new bone in the paraspinal muscle of the mouse to obtain spinal fusion. The extent and quantity of this newly formed bone can be monitored by controlling the duration of rhBMP-2 gene expression.

scholarly journals Dental Pulp Mesenchymal Stem Cells as a Treatment for Periodontal Disease in Older Adults

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Beatriz Hernández-Monjaraz ◽  
Edelmiro Santiago-Osorio ◽  
Edgar Ledesma-Martínez ◽  
Itzen Aguiñiga-Sánchez ◽  
Norma Angélica Sosa-Hernández ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Periodontal Disease ◽  
Dental Pulp ◽  
Alveolar Bone ◽  
Statistical Significance ◽  
Collagen Scaffold ◽  
Control Group ◽  
Mineral Density

Periodontal disease (PD) is one of the main causes of tooth loss and is related to oxidative stress and chronic inflammation. Although different treatments have been proposed in the past, the vast majority do not regenerate lost tissues. In this sense, the use of dental pulp mesenchymal stem cells (DPMSCs) seems to be an alternative for the regeneration of periodontal bone tissue. A quasi-experimental study was conducted in a sample of 22 adults between 55 and 64 years of age with PD, without uncontrolled systemic chronic diseases. Two groups were formed randomly: (i) experimental group (EG) n=11, with a treatment based on DPMSCs; and a (ii) control group (CG) n=11, without a treatment of DPMSCs. Every participant underwent clinical and radiological evaluations and measurement of bone mineral density (BMD) by tomography. Saliva samples were taken as well, to determine the total concentration of antioxidants, superoxide dismutase (SOD), lipoperoxides, and interleukins (IL), before and 6 months after treatment. All subjects underwent curettage and periodontal surgery, the EG had a collagen scaffold treated with DPMSCs, while the CG only had the collagen scaffold placed. The EG with DPMSCs showed an increase in the BMD of the alveolar bone with a borderline statistical significance (baseline 638.82±181.7 vs. posttreatment 781.26±162.2 HU, p=0.09). Regarding oxidative stress and inflammation markers, salivary SOD levels were significantly higher in EG (baseline 1.49±0.96 vs. 2.14±1.12 U/L posttreatment, p<0.05) meanwhile IL1β levels had a decrease (baseline 1001.91±675.5vs. posttreatment 722.3±349.4 pg/ml, p<0.05). Our findings suggest that a DPMSCs treatment based on DPMSCs has both an effect on bone regeneration linked to an increased SOD and decreased levels of IL1β in aging subjects with PD.

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