Tumor necrosis factor increases transcription of the heparin-binding epidermal growth factor-like growth factor gene in vascular endothelial cells - PubMed (original) (raw)

. 1992 May 15;267(14):9467-9.

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Tumor necrosis factor increases transcription of the heparin-binding epidermal growth factor-like growth factor gene in vascular endothelial cells

M Yoshizumi et al. J Biol Chem. 1992.

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Abstract

Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a recently identified, potent vascular smooth muscle cell (SMC) mitogen of macrophage origin. To determine whether this gene is transcribed and regulated in vascular endothelial cells, we measured HB-EGF mRNA levels in human umbilical vein endothelial cells (HUVEC) by RNA blot analysis with an HB-EGF cDNA probe. The base-line level of HB-EFG mRNA in HUVEC in culture was low. However, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta markedly increased HB-EGF mRNA levels in HUVEC by 12- and 7-fold, respectively, and induction of the gene by TNF-alpha was both dose- and time-dependent. In response to TNF-alpha, HB-EGF mRNA levels quickly increased and peaked at 1 h, indicating that HB-EGF belongs to the family of immediate early genes. In nuclear run-off experiments, TNF-alpha increased the rate of HB-EGF gene transcription by 3.2-fold. To our knowledge this is the first demonstration that the HB-EGF gene is transcribed in vascular endothelial cells. The inducible transcription of this potent SMC mitogen gene in endothelial cells suggests that HB-EGF may have an important role in the pathogenesis of atherosclerosis.

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