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VEGF regulates FGF-2 and TGF-beta1 expression in injury endothelial cells and mediates smooth muscle cells proliferation and migration.
Microvasc Res. 2009 Mar; 77(2):134-42.MR

Abstract

BACKGROUND

Vascular endothelial growth factor (VEGF) is implicated in the development of restenosis after percutaneous transluminal coronary angioplasty (PTCA) as well as atherosclerosis. The purpose of our study was: 1) to evaluate the expression of endothelial cell (EC) fibroblast growth factor 2 (FGF-2) and transforming growth factor beta1 (TGF-beta1) mRNA expression following vascular injury and VEGF modulation and 2) to assess whether VEGF indirectly stimulates smooth muscle cell (SMC) migration and proliferation via growth factors released by injured EC.

METHODS

Bovine aortic endothelial cells (BAEC) were cultured to near confluency and were serum starved. Linear wounds were made in medium with and without VEGF. FGF-2 and TGF-beta1 mRNA expression were evaluated. Bovine aortic organ culture experiments were also carried out and growth factor expression was assessed. SMC proliferation and migration was assessed in response to EC injury medium with/without VEGF.

RESULTS

EC injury in the presence of VEGF increased FGF-2 mRNA. EC injury also induced TGF-beta1 mRNA expression; however VEGF inhibited TGF-beta1 mRNA expression in both injured and noninjured ECs. VEGF increased FGF-2 mRNA stability and did not alter TGF-beta1 mRNA stability. SMC proliferation and migration was found to be induced by injured EC media and injury EC medium with VEGF, respectively

CONCLUSIONS

The results demonstrate that 1) VEGF indirectly stimulates SMC proliferation and migration through stimulation of the expression of FGF-2 and 2) VEGF inhibits the expression of TGF-beta1 released by EC. Theses data further suggest an integral role for FGF-2 and TGF-beta1 in wound repair.

Authors+Show Affiliations

Harbin Medical University, 194 Xuefu Lu, Harbin 150081, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18948122

Citation

Li, Dongmei, et al. "VEGF Regulates FGF-2 and TGF-beta1 Expression in Injury Endothelial Cells and Mediates Smooth Muscle Cells Proliferation and Migration." Microvascular Research, vol. 77, no. 2, 2009, pp. 134-42.
Li D, Zhang C, Song F, et al. VEGF regulates FGF-2 and TGF-beta1 expression in injury endothelial cells and mediates smooth muscle cells proliferation and migration. Microvasc Res. 2009;77(2):134-42.
Li, D., Zhang, C., Song, F., Lubenec, I., Tian, Y., & Song, Q. H. (2009). VEGF regulates FGF-2 and TGF-beta1 expression in injury endothelial cells and mediates smooth muscle cells proliferation and migration. Microvascular Research, 77(2), 134-42. https://doi.org/10.1016/j.mvr.2008.09.007
Li D, et al. VEGF Regulates FGF-2 and TGF-beta1 Expression in Injury Endothelial Cells and Mediates Smooth Muscle Cells Proliferation and Migration. Microvasc Res. 2009;77(2):134-42. PubMed PMID: 18948122.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - VEGF regulates FGF-2 and TGF-beta1 expression in injury endothelial cells and mediates smooth muscle cells proliferation and migration. AU - Li,Dongmei, AU - Zhang,Cuili, AU - Song,F, AU - Lubenec,I, AU - Tian,Ye, AU - Song,Q H, Y1 - 2008/10/02/ PY - 2007/12/24/received PY - 2008/09/11/revised PY - 2008/09/12/accepted PY - 2008/10/25/entrez PY - 2008/10/25/pubmed PY - 2009/7/14/medline SP - 134 EP - 42 JF - Microvascular research JO - Microvasc Res VL - 77 IS - 2 N2 - BACKGROUND: Vascular endothelial growth factor (VEGF) is implicated in the development of restenosis after percutaneous transluminal coronary angioplasty (PTCA) as well as atherosclerosis. The purpose of our study was: 1) to evaluate the expression of endothelial cell (EC) fibroblast growth factor 2 (FGF-2) and transforming growth factor beta1 (TGF-beta1) mRNA expression following vascular injury and VEGF modulation and 2) to assess whether VEGF indirectly stimulates smooth muscle cell (SMC) migration and proliferation via growth factors released by injured EC. METHODS: Bovine aortic endothelial cells (BAEC) were cultured to near confluency and were serum starved. Linear wounds were made in medium with and without VEGF. FGF-2 and TGF-beta1 mRNA expression were evaluated. Bovine aortic organ culture experiments were also carried out and growth factor expression was assessed. SMC proliferation and migration was assessed in response to EC injury medium with/without VEGF. RESULTS: EC injury in the presence of VEGF increased FGF-2 mRNA. EC injury also induced TGF-beta1 mRNA expression; however VEGF inhibited TGF-beta1 mRNA expression in both injured and noninjured ECs. VEGF increased FGF-2 mRNA stability and did not alter TGF-beta1 mRNA stability. SMC proliferation and migration was found to be induced by injured EC media and injury EC medium with VEGF, respectively CONCLUSIONS: The results demonstrate that 1) VEGF indirectly stimulates SMC proliferation and migration through stimulation of the expression of FGF-2 and 2) VEGF inhibits the expression of TGF-beta1 released by EC. Theses data further suggest an integral role for FGF-2 and TGF-beta1 in wound repair. SN - 1095-9319 UR - https://www.unboundmedicine.com/medline/citation/18948122/VEGF_regulates_FGF_2_and_TGF_beta1_expression_in_injury_endothelial_cells_and_mediates_smooth_muscle_cells_proliferation_and_migration_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0026-2862(08)00144-1 DB - PRIME DP - Unbound Medicine ER -