Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells.

Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Research Abstract Details 

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Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Abstract Text:

Kristina ,Amina F Zebboudj,Yucheng Yao,Than S Lin,Alejandra Torres,

Matrix GLA protein (MGP) is expressed in endothelial cells (EC), and MGP deficiency results in developmental defects suggesting involvement in EC function. To determine the role of MGP in EC, we cultured bovine aortic EC with increasing concentrations of human MGP (hMGP) for 24 h. The results showed increased proliferation, migration, tube formation, and increased release of vascular endothelial growth factor-A (VEGF-A) and basic fibroblast growth factor (bFGF). HMGP, added endogenously or transiently expressed, increased VEGF gene expression dose-dependently as determined by real-time PCR. To determine the mechanism by which hMGP increased VEGF expression, we studied the effect of MGP on the activity of transforming growth factor (TGF)-beta1 compared with that of bone morphogenetic protein (BMP)-2 using transfection assays with TGF-beta- and BMP-response element reporter genes. Our results showed a strong enhancement of TGF-beta1 activity by hMGP, which was paralleled by increased VEGF expression. BMP-2 activity, on the other hand, was inhibited by hMGP. Neutralizing antibodies to TGF-beta blocked the effect of MGP on VEGF expression. The enhanced TGF-beta1 activity specifically activated the Smad1/5 pathway indicating that the TGF-beta receptor activin-like kinase 1 (ALK1) had been stimulated. It occurred without changes in expression of TGF-beta1 or ALK1 and was mimicked by transfection of constitutively active ALK1, which increased VEGF expression. Expression of VEGF and MGP was induced by TGF-beta1, but the induction of MGP preceded that of VEGF, consistent with a promoting effect on VEGF expression. Together, the results suggest that MGP plays a role in EC function, altering the response to TGF-beta superfamily growth factors.

Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Publishing Authors By Initials

K ,AF Zebboudj,Y Yao,TS Lin,A Torres,

For similar peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research abstracts see: peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research

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Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: The Journal of biological chemistry

VOLUME: 279

Page Numbers: 52904-13

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 27

MONTH: 09

YEAR: 2004

Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985121

Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Keywords Mesh Terms:

KEYWORDS: Vascular Endothelial Growth Factor A

MESH TERMS: metabolism

Chemical & Substance for Abstract: Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells. Information

Substance Name: Luciferases

Registry Number: EC 1.13.12.-

Grant and Affiliation Information for Matrix GLA protein stimulates VEGF expression through increased transforming growth factor-beta1 activity in endothelial cells.

AFFILIATION: Division of Cardiology, David Geffen School of Medicine, University of California, Box 951679, Rm. 47-123 CHS, Los Angeles, CA 90095-1679, USA. kbostrom@mednet.ucla.edu

Country: United States

AGENCY: United States NHLBI

GRANT: HL04270

ACRONYM: HL

MEDLINETA: J Biol Chem

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