Lentivirus-mediated cyclooxygenase 2 and aggrecanase 1 silencing and insulin-like growth factor 1 overexpression in human bone marrow mesenchymal stem cells
10.3969/j.issn.2095-4344.2015.10.003
- VernacularTitle:骨髓间充质干细胞中环氧化酶2及聚蛋白多糖酶1沉默与胰岛素样生长因子1过表达
- Author:
Yuqi YUAN
;
Haining ZHANG
;
Xia KONG
;
Aihua SUI
;
Yingzhen WANG
- Publication Type:Journal Article
- Keywords:
Mesenchymal Stem Cels;
Lentivirus Infections;
Cyclooxygenase 2;
Insulin-Like Growth Factor I
- From:
Chinese Journal of Tissue Engineering Research
2015;(10):1488-1494
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Cyclooxygenase 2, aggrecanase 1, and insulin-like growth factor 1 are involved in pathological injury of the articular cartilage. OBJECTIVE:To observe the expression of shRNA vectors carrying cyclooxygenase 2, aggrecanase 1 and overexpression vectors carrying insulin-like growth factor 1 in bone marrow mesenchymal stem cels. METHODS:Lentiviral vectors carrying the silencing gene cyclooxygenase 2, aggrecanase 1, the over-expressing gene insulin-like growth factor 1 and binding green fluorescent protein were constructed with recombinant lentiviral technology, and then the recombinant lentiviral vectors were used to transfect passage 3 human bone marrow mesenchymal stem cels culturedin vitro (experimental group). The human bone marrow mesenchymal stem cels transfected with no target gene lentivirals were used as negative control group. The human bone marrow mesenchymal stem cels transfected with no treatment served as blank group. RESULTS AND CONCLUSION:Cyclooxygenase 2 and aggrecanase 1 transfected in human bone marrow mesenchymal stem cels were significantly inhibited at gene and protein levels, while the expression of insulin-like growth factor 1 was increased significantly at gene and protein levels. We confirmed that cyclooxygenase 2 and aggrecanase 1 were successfuly silenced while insulin-like growth factor 1 overexpressed by using lentiviral vectors in human bone marrow mesenchymal stem cels, which brings a new hope for the systemic gene treatment of arthritis.