Induction of vascular endothelial growth factor expression in synovial fibroblasts by prostaglandin E and interleukin‐1: a potential mechanism for inflammatory angiogenesis

FEBS Letters

Ben-Av, Pazit¹  Wilder, Ronald L.²  Hla, Timothy¹  Crofford, Leslie J.³ 

[1] Department of Molecular Biology, Holland Laboratory, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA;NIAMS, NIH, Bethesda, MD, USA;Department of Internal Medicine, Division of Rheumatology, University of Michigan School of Medicine, Ann Arbor, MI, USA

关键词: Angiogenesis;    Interleukin-1α;    Prostaglandin E2;    Rheumatoid arthritis;    Vascular endothelial growth factor;    IL-1α;    interleukin-1;    PGE1;    prostaglandin E1;    PGE2;    prostaglandin E2;    RA;    rheumatoid arthritis;    RT-PCR;    reverse transcriptase-polymerase chain reaction;    VEGF;    vascular endothelial growth factor;   

DOI  :  10.1016/0014-5793(95)00956-A

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Inflammatory mediators such as prostaglandin E₂ (PGE₂) and interleukin-1 (IL-1) induce angiogenesis by yet undefined mechanisms. We demonstrate that PGE₂ and IL-1 induces the expression of vascular endothelial growth factor (VEGF), a selective angiogenic factor by rheumatoid synovial fibroblast cells. Transcripts for the EP₁ and EP₂, subtypes of PGE receptors are expressed in synovial fibroblasts. Activators of protein kinase A pathway stimulated the expression of VEGF whereas down-regulation of protein kinase C did not influence the PGE effect, suggesting that signalling from the EP₂ receptor via the protein kinase A pathway is important. The induction of VEGF expression by PGE₂ and interleukin-1α a may be an important mechanism in inflammatory angiogenesis.

【 授权许可】

Unknown