Bone Marrow Mesenchymal Stem Cells Induce Angiogenesis and Promote Bladder Cancer Growth in a Rabbit Model

2010 ◽  
Vol 84 (1) ◽  
pp. 94-99 ◽  
Author(s):  
Keqin Zhang ◽  
Benkang Shi ◽  
Jun Chen ◽  
Dongqing Zhang ◽  
Yaofeng Zhu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Bladder Cancer ◽  
Mesenchymal Stem Cells ◽  
Rabbit Model ◽  
Cancer Growth ◽  
Marrow Mesenchymal Stem Cells

EVALUATION OF THREE DIMENSIONAL CONSTRUCT ENGINEERED FROM POLY(LACTIC-CO-GLYCOLIC ACID)/FIBRIN HYBRID SCAFFOLD USING RABBIT BONE MARROW MESENCHYMAL STEM CELLS FOR OSTEOCHONDRAL DEFECT REPAIR

2015 ◽  
Vol 77 (25) ◽  
Author(s):  
Rozlin Abdul Rahman ◽  
Norhamiza Mohamad Sukri ◽  
Noorhidayah Md Nazir ◽  
Muhammad Aa’zamuddin Ahmad Radzi ◽  
Ahmad Hafiz Zulkifly ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Glycolic Acid ◽  
Osteochondral Defect ◽  
Rabbit Model ◽  
Three Dimensional ◽  
Marker Genes ◽  
Repair Capacity ◽  
Marrow Mesenchymal Stem Cells

Articular cartilage has poor repair capacity due to its avascular and aneural properties and has relatively few cells. This study investigated the ability of autologous implantation approach using three dimensional (3D) constructs engineered from bone marrow mesenchymal stem cells (BMSCs) seeded on poly(lactic-co-glycolic acid) (PLGA) with or without fibrin as cells carrier for the repair of osteochondral defect in rabbit model. The engineered 3D constructs – PLGA/Fibrin/BMSCs and PLGA/BMSCs – were cultured for 3 weeks in vitro and implanted autologously to the osteochondral defect created in the rabbit knee. The in vivo constructs were harvested and evaluated by means of gross observation, histology assessment, gene expression study, sulphated glycosaminoglycan (sGAG) production assay and biomechanical evaluation at 6 and 12 weeks post implantation. The results showed that the osteochondral defects treated with the PLGA/Fibrin/BMSCs constructs exhibited better repairment, more cartilaginous extracellular matrix, higher sGAG production, superior compressive strength and more intense expression of chondrogenic marker genes than the PLGA/BMSCs group. This study suggested that the PLGA/Fibrin/BMSCs has the potential to treat osteochondral defect and may be presented as a viable therapeutic option for those who would be in need from the life-extending benefits of tissue replacement or repair.

Fibrin Glue with Autogenic Bone Marrow Mesenchymal Stem Cells for Urethral Injury Repair in Rabbit Model

2012 ◽  
Vol 18 (23-24) ◽  
pp. 2507-2517 ◽  
Author(s):  
Kai Wang ◽  
Yong Guan ◽  
Yi Liu ◽  
Meifeng Zhu ◽  
Ting Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Fibrin Glue ◽  
Rabbit Model ◽  
Urethral Injury ◽  
Injury Repair ◽  
Marrow Mesenchymal Stem Cells

scholarly journals Human Bone Marrow Mesenchymal Stem Cells Promote Gastric Cancer Growth via Regulating c-Myc

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Bin Chen ◽  
Jing Yu ◽  
Qianqian Wang ◽  
Yuanyuan Zhao ◽  
Li Sun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Clinical Application ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Cancer Growth ◽  
Gastric Cancer Cells ◽  
Marrow Mesenchymal Stem Cells

The clinical application of human bone marrow mesenchymal stem cells (hBM-MSCs) has generated a great deal of interest because of their potential use in regenerative medicine and tissue engineering. However, safety concerns over hBM-MSCs limit their clinical application. In this study, we observed that hBM-MSC-conditioned medium (hBM-MSC-CM) promotes gastric cancer development via upregulation of c-Myc. Our results showed that c-Myc was upregulated in MGC-803 and BGC-823 cells after hBM-MSC-CM treatment. Moreover, we found that the c-Myc inhibitor JQ1 and c-Myc siRNA decreased the expression of c-Myc in hBM-MSC-CM-treated tumor cells in vitro. Additionally, hBM-MSC-CM enhanced the migration and glucose uptake of gastric cancer cells. In vivo studies showed that JQ1 inhibited hBM-MSC-CM-induced gastric cancer growth. These results indicated that hBM-MSC-CM induced gastric cancer growth via upregulation of c-Myc, which may be a potential risk factor and/or a therapeutic target for clinical applications.

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