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VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) induced intimal hyperplasia in carotid arteries.
Eur J Clin Invest. 2005 Nov; 35(11):669-76.EJ

Abstract

BACKGROUND

The role of vascular endothelial growth factors (VEGFs) in intimal hyperplasia and atherogenesis remains unknown. Several studies have suggested that some members of the VEGF family reduce intimal hyperplasia, but others have proposed that VEGFs accelerate restenosis and atherosclerosis. This investigation conducted a comparative study with adenoviruses encoding different VEGFs in a rabbit carotid artery collar model of intimal hyperplasia in order to analyze the role of VEGFs in the formation of intimal hyperplasia.

MATERIALS AND METHODS

Intimal hyperplasia was induced in the carotid arteries of cholesterol fed New Zealand White rabbits using a silastic collar. Adenoviral vectors encoding VEGF-A, VEGF-B, VEGF-C, VEGF-C(DeltaNDeltaC), VEGF-D and VEGF-D(DeltaNDeltaC) were delivered to the adventitia using the collar as a gene delivery device. Adeno-LacZ was used as a control.

RESULTS

A significant (P < 0.01) increase in the intima/media ratio was observed in the arteries transduced with VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC). There was a significant increase in the number of proliferating cells in the adventitia, media and intima of the VEGF-A, VEGF-D and the VEGF-D(DeltaNDeltaC) transduced arteries. The majority of medial smooth muscle cells in these arteries had a synthetic phenotype. The presence of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the VEGF-A, VEGF-D and the VEGF-D(DeltaNDeltaC) transduced arteries was significantly increased. A significant positive correlation was observed between adventitial angiogenesis and intimal hyperplasia.

CONCLUSIONS

Adventitial delivery of adenoviruses encoding VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) increased intimal hyperplasia in the rabbit collar model. Adventitial angiogenesis correlated positively with the intimal hyperplasia. These results indicated that efficient adventitial production of VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) can cause thickening of the inner layer of the artery in rabbits.

Authors+Show Affiliations

University of Kuopio, Kuopio, Finland.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16269016

Citation

Bhardwaj, S, et al. "VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) Induced Intimal Hyperplasia in Carotid Arteries." European Journal of Clinical Investigation, vol. 35, no. 11, 2005, pp. 669-76.
Bhardwaj S, Roy H, Heikura T, et al. VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) induced intimal hyperplasia in carotid arteries. Eur J Clin Invest. 2005;35(11):669-76.
Bhardwaj, S., Roy, H., Heikura, T., & Ylä-Herttuala, S. (2005). VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) induced intimal hyperplasia in carotid arteries. European Journal of Clinical Investigation, 35(11), 669-76.
Bhardwaj S, et al. VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) Induced Intimal Hyperplasia in Carotid Arteries. Eur J Clin Invest. 2005;35(11):669-76. PubMed PMID: 16269016.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) induced intimal hyperplasia in carotid arteries. AU - Bhardwaj,S, AU - Roy,H, AU - Heikura,T, AU - Ylä-Herttuala,S, PY - 2005/11/5/pubmed PY - 2006/8/22/medline PY - 2005/11/5/entrez SP - 669 EP - 76 JF - European journal of clinical investigation JO - Eur. J. Clin. Invest. VL - 35 IS - 11 N2 - BACKGROUND: The role of vascular endothelial growth factors (VEGFs) in intimal hyperplasia and atherogenesis remains unknown. Several studies have suggested that some members of the VEGF family reduce intimal hyperplasia, but others have proposed that VEGFs accelerate restenosis and atherosclerosis. This investigation conducted a comparative study with adenoviruses encoding different VEGFs in a rabbit carotid artery collar model of intimal hyperplasia in order to analyze the role of VEGFs in the formation of intimal hyperplasia. MATERIALS AND METHODS: Intimal hyperplasia was induced in the carotid arteries of cholesterol fed New Zealand White rabbits using a silastic collar. Adenoviral vectors encoding VEGF-A, VEGF-B, VEGF-C, VEGF-C(DeltaNDeltaC), VEGF-D and VEGF-D(DeltaNDeltaC) were delivered to the adventitia using the collar as a gene delivery device. Adeno-LacZ was used as a control. RESULTS: A significant (P < 0.01) increase in the intima/media ratio was observed in the arteries transduced with VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC). There was a significant increase in the number of proliferating cells in the adventitia, media and intima of the VEGF-A, VEGF-D and the VEGF-D(DeltaNDeltaC) transduced arteries. The majority of medial smooth muscle cells in these arteries had a synthetic phenotype. The presence of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the VEGF-A, VEGF-D and the VEGF-D(DeltaNDeltaC) transduced arteries was significantly increased. A significant positive correlation was observed between adventitial angiogenesis and intimal hyperplasia. CONCLUSIONS: Adventitial delivery of adenoviruses encoding VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) increased intimal hyperplasia in the rabbit collar model. Adventitial angiogenesis correlated positively with the intimal hyperplasia. These results indicated that efficient adventitial production of VEGF-A, VEGF-D and VEGF-D(DeltaNDeltaC) can cause thickening of the inner layer of the artery in rabbits. SN - 0014-2972 UR - https://www.unboundmedicine.com/medline/citation/16269016/VEGF_A_VEGF_D_and_VEGF_D_DeltaNDeltaC__induced_intimal_hyperplasia_in_carotid_arteries_ L2 - https://doi.org/10.1111/j.1365-2362.2005.01555.x DB - PRIME DP - Unbound Medicine ER -