RT Journal Article
SR Electronic
T1 The effect of radionucleide hNIS gene therapy and lentivirus-mediated RNAi HexokinaseII in rat aortic vascular smooth muscle A7r5 cell line
JF Journal of Nuclear Medicine
JO J Nucl Med
FD Society of Nuclear Medicine
SP 1684
OP 1684
VO 51
IS supplement 2
A1 Hwang, Mi-hye
A1 Kim, Jung Eun
A1 Lee, You La
A1 Jeon, Yong Hyun
A1 Jeong, Shin Young
A1 Lee, Sang-Woo
A1 Ahn, Byeong-Cheol
A1 Lee, Jaetae
YR 2010
UL http://jnm.snmjournals.org/content/51/supplement_2/1684.abstract
AB 1684 Objectives Abnormal proliferation and migration of vascular smooth muscle cells(VSMCs) are important in pathogenesis of atherosclerosis. Sodium/iodide symporter(NIS) has been used radionucleide therapeutic gene for cancer. RNAi of HKII can be tool inhibit cell proliferation. Radionucleide hNIS gene therapy and HKII-shRNA for proliferation of VSMCs. This study was undertaken to clarify the effect of lentivirus-mediated HKII-shRNA gene expression on A7r5-NL cells. Methods A7r5 cells were stably transfected with dual expression vector of hNIS and luciferase gene(pIRES-hNIS-Luc). Cells stably expressing the hNIS gene and luciferase gene were A7r5-NL produced, and the expression of the hNIS gene and luciferase gene was examined by I-125 uptake,luciferase assay and RT-PCR. Recombinant lentivirus producing HKII-shRNA was prepared. The effects of the lentivirus HKII-shRNA on protein and mRNA expression of HKII examined by western blot,RT-PCR. Cell growth was determined using MTT assay and effect of I-131 on A7r5-NL cells was also evaluation. Results We established A7r5 cells which stably expressed hNIS and luciferase genes. Lentivirus-mediated RNAi effectively reduced endogenous HKII expression and downregulation of HKII in A7r5-NL cells and significantly inhibitied cell growth of A7r5-NL cells. A7r5-NL cells higher I-125 uptake and RLU compared to parent cell. Conclusions Radionucleide hNIS gene therapy and the lentivirus-HKII-shRNA suppressed cell proliferation of A7r5-NL. Therefore both therapies can be applied to treat atherosclerosis or prevent recurrence of atherosclerotic process by inhibiting VSMC proliferation