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e0704 The study of effect of angiotensin II on the biological behaviour of rat vascular smooth muscle cells in vitro

H. Guoxiang, L. Jianping, Jing Tao

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Abstract

Objective To study the effect of Angiotensin II on the roliferation, migration and apoptosis of vascular smooth muscle cell (VSMC) in rats. Methods The recombinant adenoviral vector, AdCMV-AT2R, containing rat AT2 receptor gene was constructed by homologous recombination, and then it was used to transfer AT2 receptor gene to rat VSMC in vitro. The expression of AT2R mRNA was detected by RT-PCR and the rate of expression in VSMC was determined by flow cytometer. Cell proliferation was determined by incorporation of bromodeoxyuridine (BrdU). The modified Boyden9s chamber method was used to test the migration of VSMC. Apoptosis was quantified by flow cytometer. Results RT-PCR showed that the expression of AT2R mRNA increased obviously in transferred VSMC, and the peak value of expression rate was about 89.51% at 48 h. When the expression of AT2R was at peak value, the OD value of BrdU incorporation were reduced by 51.6% (p<0.01), and the number of VSMC migration was also decreased by 62.2% (p<0.05). The ratio of apoptosis in VSMC was increased from 7.6±1.6% in control group to 32.1±5.5% in treated group. Conclusion The results indicated that the expression of AT2R can inhibit the proliferation and migration of rat VSMC and induce its apoptosis.

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Objective To study the effect of Angiotensin II on the roliferation, migration and apoptosis of vascular smooth muscle cell (VSMC) in rats. Methods The recombinant adenoviral vector, AdCMV-AT2R, containing rat AT2 receptor gene was constructed by homologous recombination, and then it was used to transfer AT2 receptor gene to rat VSMC in vitro. The expression of AT2R mRNA was detected by RT-PCR and the rate of expression in VSMC was determined by flow cytometer. Cell proliferation was determined by incorporation of bromodeoxyuridine (BrdU). The modified Boyden9s chamber method was used to test the migration of VSMC. Apoptosis was quantified by flow cytometer. Results RT-PCR showed that the expression of AT2R mRNA increased obviously in transferred VSMC, and the peak value of expression rate was about 89.51% at 48 h. When the expression of AT2R was at peak value, the OD value of BrdU incorporation were reduced by 51.6% (p<0.01), and the number of VSMC migration was also decreased by 62.2% (p<0.05). The ratio of apoptosis in VSMC was increased from 7.6±1.6% in control group to 32.1±5.5% in treated group. Conclusion The results indicated that the expression of AT2R can inhibit the proliferation and migration of rat VSMC and induce its apoptosis.

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Available abstract

Objective To study the effect of Angiotensin II on the roliferation, migration and apoptosis of vascular smooth muscle cell (VSMC) in rats. Methods The recombinant adenoviral vector, AdCMV-AT2R, containing rat AT2 receptor gene was constructed by homologous recombination, and then it was used to transfer AT2 receptor gene to rat VSMC in vitro. The expression of AT2R mRNA was detected by RT-PCR and the rate of expression in VSMC was determined by flow cytometer. Cell proliferation was determined by incorporation of bromodeoxyuridine (BrdU). The modified Boyden9s chamber method was used to test the migration of VSMC. Apoptosis was quantified by flow cytometer. Results RT-PCR showed that the expression of AT2R mRNA increased obviously in transferred VSMC, and the peak value of expression rate was about 89.51% at 48 h. When the expression of AT2R was at peak value, the OD value of BrdU incorporation were reduced by 51.6% (p<0.01), and the number of VSMC migration was also decreased by 62.2% (p<0.05). The ratio of apoptosis in VSMC was increased from 7.6±1.6% in control group to 32.1±5.5% in treated group. Conclusion The results indicated that the expression of AT2R can inhibit the proliferation and migration of rat VSMC and induce its apoptosis.

Key concepts: Vascular smooth muscle, Apoptosis, Angiotensin II, In vitro, Receptor, Bromodeoxyuridine, Flow cytometry, Internal medicine

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