Human tissue kallikrein 1 gene delivery inhibits PDGF-BB-induced vascular smooth muscle cells proliferation and upregulates the expressions of p27Kip1 and p2lCip1

Tissue kallikrein 1 cleaves kininogen substrate to produce vasoactive kinin peptides that have been implicated in inhibiting neointimal hyperplasia in rat carotid arteries after balloon injury. However, its effects on the proliferation, cell cycle and its mechanisms, for example, cyclin-dependent ki...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2012, Vol.360 (1-2), p.363-371
Main Authors: Yu, Hui-Zhen, Xie, Liang-di, Zhu, Peng-li, Xu, Chang-sheng, Wang, Hua-jun
Format: Article
Language:English
Subjects:
Animals
Biochemistry
Biomedical and Life Sciences
Cardiology
Cell Proliferation
Cells, Cultured
Cyclin-Dependent Kinase Inhibitor p21 - genetics
Cyclin-Dependent Kinase Inhibitor p21 - metabolism
Cyclin-Dependent Kinase Inhibitor p27 - genetics
Cyclin-Dependent Kinase Inhibitor p27 - metabolism
G1 Phase Cell Cycle Checkpoints
Gene Expression
Humans
Life Sciences
Medical Biochemistry
Mitogens - pharmacology
Muscle, Smooth, Vascular - cytology
Myocytes, Smooth Muscle - drug effects
Myocytes, Smooth Muscle - physiology
Oncology
Proto-Oncogene Proteins c-sis - pharmacology
Rats
Rats, Inbred SHR
Recombinant Proteins - genetics
Recombinant Proteins - metabolism
Tissue Kallikreins - genetics
Tissue Kallikreins - metabolism
Up-Regulation
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Summary:Tissue kallikrein 1 cleaves kininogen substrate to produce vasoactive kinin peptides that have been implicated in inhibiting neointimal hyperplasia in rat carotid arteries after balloon injury. However, its effects on the proliferation, cell cycle and its mechanisms, for example, cyclin-dependent kinase inhibitors, p27 Kip1 and p2l Cip1 in vascular biology are poorly understood. The objective of this study was to explore the effects of human tissue kallikrein 1 (hTK1) mediated by recombinant adenovirus (Ad-hTK1) on proliferation and cell cycle of vascular smooth muscle cells (VSMCs) derived from spontaneously hypertensive rats induced by platelet-derived growth factor-BB (PDGF-BB) in vitro. The results showed that, within a given multiplicity of infection (MOI) and time, the hTK1 gene delivery inhibited PDGF-BB-stimulating VSMCs growth in a concentration-dependent (20–100 MOI) and time-dependent (2–5 days) manner by cell counting, with a peak inhibition rate at 36.3% at 72 h ( P  
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-011-1076-y