2010 Fiscal Year Final Research Report
Transfection of Kir6. 2 channel genes into native vascular smooth muscle using sonoporation
| Project/Area Number |
20300178
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical systems
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| Research Institution | Saga University (2010)
Kyushu University (2008-2009) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
INAI Tetsuichiro 福岡歯科大学, 歯学部, 教授 (00264044)
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| Co-Investigator(Renkei-kenkyūsha) |
KODAMA Tetsuya 東北大学, 大学院・医工学研究科, 教授 (40271986)
ITO Hiroyuki 九州大学, 大学病院, 講師 (10346778)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 分子薬理学 / 電気生理学 / 分子生物学 / DDS / ナノ医工学 |
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| Research Abstract |
The combination of ultrasound and nano-bubbles coated with lipid bilayers(i. e. hybrid nano-bubbles) induces transient membrane permeability, leading to direct delivery of exogenous molecules(such as plasmid, siRNA, anticancer drugs etc.) into cells with minimal invasion. This method is generally termed as to be a sonoporation technique. When Kir6. 2(inwardly-rectifying K^+ channel family 6 subtype 2) genes have transfected into native vascular smooth muscle layers of mouse aorta by use of sonoporation, RT-PCR analysis revealed the expression of Kir6. 2 transcripts in vascular smooth muscle. When Kir6. 2 genes, tagging with Myc-genes, were transfected into native smooth muscle layers using sonoporation, immunohistochemical studies have revealed that Kir6. 2 and Myc proteins were co-expressed in vascular smooth muscle cells. The phenylephrine-induced contraction of mouse aorta was significantly reduced after the treatment of Kir6. 2 gene-sonoporation, hyperpolaring the membrane potentials of vascular smooth muscle.
These results suggest that Kir6. 2 genes were functionally expressed in mouse vascular smooth muscles, causing a vascular relaxation due to the activity of Kir6. 2. Thus, we have succeeded to establish the novel gene-transfected method.
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