Decoy oligodeoxynucleotides and neointimal hyperplasia following balloon injury of rat common carotid artery

doi:10.3969/j.issn.2095-4344.2013.07.017

Abstract

Abstract:

BACKGROUND: Restenosis following percutaneous coronary intervention is still a clinically serious problem which negatively affects the long-term therapeutic benefit of percutaneous coronary intervention.
OBJECTIVE: To investigate the effect of Egr-1 decoy oligodeoxynucleotides via intracerebroventricular injection on the neointima after carotid balloon injury and to primarily study its mechanism of inhibiting neiointimal hyperplasia, thus providing a new prospect to find a new target of vascular remodeling and restenosis.
METHODS: Endothelial denuded carotid models were prepared in rats by balloon withdrawal injury with the help of 2F Fogarty. Then Egr-1 decoy oligodeoxynucleotides were injected into injured vascular subsection which was mediated by Fugene6 transfection reagent. The extent of neointimal hyperplasia and the expression of Cyclin D1 were detected by hematoxylin-eosin staining and immunohistochemistry, respectively.
RESULTS AND CONCLUSION: Neointimal hyperplasia was significantly inhibited by Egr-1 decoy oligodeoxynucleotides. The expression of Cyclin D1, which was dramatically increased after balloon injury of rat common carotid artery, was significantly down-regulated by Egr-1 decoy oligodeoxynucleotides. Egr-1 decoy oligodeoxynucleotides may inhibit neointimal hyperplasia following balloon injury of rat common carotid artery via down-regulation of Cyclin D1.

Key words: tissue construction, tissue construction and bioactive factor, growth response factor, carotid artery, injury, oligodeoxynucleotides, Cyclin D1, balloon injury, restenosis, the National Natural Science Foundation of China, tissue construction photographs-containing paper

CLC Number:

R318

Wang Shuai, Liu Gui-nan, Wang Tai-ran. Decoy oligodeoxynucleotides and neointimal hyperplasia following balloon injury of rat common carotid artery[J]. Chinese Journal of Tissue Engineering Research, 2013, 17(7): 1233-1237.

Figures/Tables 4

References

[1] Rupp J, Hellwig-Burgel T, Wobbe V, et al. Chlamydia pneumonia infection promotes a Proliferative phenotype in the vasculature through Egr-1activation in vitro and in vivo. J Proc Natl Acad Sci USA. 2005;102(9):3447-3452.

[2] Khachigian LM. Early growth response-1 in cardiovascular pathobiology. J Circ Res. 2006;98(2):186-191.

[3] Khachigian LM. Early growth response-1: blocking angiogenesis by shooting the messenger. J Cell Cycle. 2004;3(1):10-11.

[4] Wang L, Zheng J, Du Y, et al. Cartilage oligomeric matrix protein maintains the contractile phenotype of vascular smooth muscle cells by interacting with alpha(7)beta(1) integrin. J Circ Res. 2010;106(3):514-525.

[5] Wada Y, Suzuli J, Kawauchi M, et al. Ealy growth response factor-1and basic transcriptional element-binding Protein 2 expression in cardiac allografts. J Heart Lung Transplant. 2001;20(5):590-594.

[6] Tomita N, Azuma H, Kaneda Y, et al.Application of decoy oligodeoxynucleotides-based approach to renal diseases. J Curr Drug Targets. 2004;5(8):717-733.

[7] Ohtani K, Egashira K, Usui M, et al. Inhibition of neointimal haperplasia after balloon injury by cis-element‘decoy’ of early growth response gene-1 in hapercholesterolemic rabbits. J Gene Therpy. 2004;11(2):126-132.

[8] Tomita N, Kashihara N, Morishita R. Transcription factor decoy oligonucleotide-based therapeutic strategy for renal disease. J Clin Exp Nephrol. 2007;11(1):7-17.

[9] Usui M, Egashira K, Ohtani K, et al. Anti-monocyte chemoattractant protein-1 gene therapy inhibits restenotic changes(neointimal hyperplasia) after balloon injury in rat and monkeys. J FASEB J. 2002;16(13):1838-1840.

[10] Bonta PI, Pols TW, van Tiel CM, et al. Nuclear receptor Nurr1 is expressed in and is associated with human restenosis and inhibits vascular lesion formation in mice involving inhibition of smooth muscle cell proliferation and inflammation. J Circulation. 2010;121(18):2023-2032.

[11] Osherov AB, Gotha L, Cheema AN, et al. Proteins mediating collagen biosynthesis and accumulation in arterial repair: novel targets for anti-restenosis therapy. J Cardiovasc Res. 2011;91(1):16-26.

[12] Xiang M, Xu YJ, Liu XS, et al. Cigarette smoke extract promotes human pulmonary artery smooth muscle cells proliferation through protein kinase C alpha-dependent induction of Cyclin D1. J Chin Med J (Engl). 2010;123(24): 3663-3670.

[13] Nakagawa M, Ohno T, Maruyama R, et al. Sesquiterpene lactone suppresses vascular smooth muscle cell proliferation and migration via inhibition of cell cycle progression. J Biol Pharm Bull. 2007;30(9):1754-1757.

[14] Li F, Duman-Scheel M, Yang D, et al. Sonic hedgehog signaling induces vascular smooth muscle cell proliferation via induction of the G1 cyclin-retinoblastoma axis. J Arterioscler Thromb Vasc Biol. 2010;30(9):1787-1794.

[15] Kavurma MM, Khachigian LM. Sp1 inhibits proliferation and induces apoptosis in vascular smooth muscle cells by repressing p21WAF1/Cip1 transcription and Cyclin D1-Cdk4-p21WAF1/Cip1 complex formation. J Biol Chem. 2003;278(35):32537-32543.

[16] Wu Y, Han W, Liu GN. A DNA enzyme targeting Egr-1 inhibits rat vascular smooth muscle cell proliferation by down-regulation of Cyclin D1 and TGF-beta1. J Braz J Med Biol Res. 2010;43(1):17-24.

[17] Zhang LS, Ma HW, Greyner HJ, et al. Inhibition of cell proliferation by CD44: Akt is inactivated and EGR-1 is down-regulated. J Cell Prolif. 2010;43(4):385-395.

[18] Han W, Liu GN. EGR-1 decoy ODNs inhibit vascular smooth muscle cell proliferation and neointimal hyperplasia of balloon- injured arteries in rat. J Life Sciences. 2010;86(7-8): 234-243.