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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Yu, Huizhen Huang, Shujie Li, Feng Zhu, Pengli Xiang, Hong Zheng, Weiping |
| Description | Author Affiliation: Zhu P ( Department of Geriatrics, Fujian Provincial Hospital Key Laboratory of Geriatrics, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.); Yu H ( Department of Geriatrics, Fujian Provincial Hospital Key Laboratory of Geriatrics, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.); Huang S ( Department of Cardiology, Fujian Provincial Hospital, Fuzhou, Fujian 350001, P.R. China.); Xiang H ( Department of Geriatrics, Fujian Provincial Hospital Key Laboratory of Geriatrics, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.); Li F ( Department of Geriatrics, Fujian Provincial Hospital Key Laboratory of Geriatrics, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.); Zheng W ( Department of Geriatrics, Fujian Provincial Hospital Key Laboratory of Geriatrics, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.) |
| Abstract | Tissue kallikrein 1 (TK1) and tissue inhibitor of matrix metalloproteinase 1 (TIMP1) are important in inhibiting vascular smooth muscle cell (VSMC) proliferation and improving vascular remodeling, respectively. It was hypothesized that a combination of TK1 and TIMP1 genes, mediated by an adenovirus vector could augment or act in synergy to enhance the inhibitory effects. The promoter, mCMV carrying hTIMP1 cDNA was subcloned into pDC316hTK1 to construct a recombinant plasmid carrying hTK1 and hTIMP1 genes. Subsequently, the double gene plasmid and adenovirus backbone plasmid were packaged into HEK293A cells. Gene transcription and protein expression were examined, respectively using reverse transcriptionquantitative polymerase chain reaction (PCR) and western blotting assays. VSMC proliferation was assessed using cell counting and methylthiazolyltetrazoliuin methods. The constructed plasmid containing hTK1 and hTIMP1 genes was correctly identified by means of PCR, double digestion and sequencing analysis. The coexpression vector, AdhTK1hTIMP1 was successfully constructed and packaged into HEK293A cells. When VSMCs were transfected with the coexpression vector, the mRNA transcription and protein expression of hTK1 and hTIMP1 exhibited abundant expression in a concentrationdependent and timedependent manner, independently. In conclusion, the coexpression vector synergistically inhibited the cell growth and proliferation induced by plateletderived growth factorBB compared with the single gene vector. |
| ISSN | 17912997 |
| e-ISSN | 17913004 |
| DOI | 10.3892/mmr.2015.4198 |
| Journal | Molecular Medicine Reports |
| Issue Number | 4 |
| Volume Number | 12 |
| Language | English |
| Publisher | Spandidos Publications |
| Publisher Date | 2015-10-01 |
| Publisher Place | Greece |
| Access Restriction | Open |
| Subject Keyword | Genetic Vectors Metabolism Plasmids Tissue Inhibitor Of Metalloproteinase-1 Genetics Tissue Kallikreins Adenoviridae Animals Aorta Cytology Drug Effects Cell Culture Techniques Cell Proliferation Gene Expression Chemistry Hek293 Cells Molecular Sequence Data Muscle, Smooth, Vascular Myocytes, Smooth Muscle Proto-oncogene Proteins C-sis Pharmacology Rats, Sprague-dawley Transfection Transgenes Research Support, Non-u.s. Gov't Discipline Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology |
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