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Blood, 1 September 2000, Vol. 96, No. 5, pp. 1772-1781
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Egr-1 gene is induced by the systemic administration of the
vascular endothelial growth factor and the epidermal growth
factor
Lixin Liu,
Jo C. Tsai, and
William C. Aird
From the Department of Molecular Medicine, Beth Israel
Deaconess Medical Center, Boston, MA.
Egr-1 is a transcription factor that couples short-term
changes in the extracellular milieu to long-term changes in gene
expression. In cultured endothelial cells, the Egr-1 gene has been
shown to respond to a variety of extracellular signals. However, the
physiological relevance of these findings remains unclear. To address
this question, the growth factor-mediated response of the Egr-1 gene
under in vivo conditions was analyzed. To that end, either vascular
endothelial growth factor (VEGF) or epidermal growth factor (EGF) was
injected into the intraperitoneal cavity of mice. Growth factors were
delivered to all tissues examined, as evidenced by the widespread
distribution of I125-labeled growth factors and the
phosphorylation of their respective receptors. In Western blot analyses
of whole-tissue extracts, Egr-1 protein levels were shown to be induced
in the heart, brain, liver, and spleen of VEGF-treated mice, and in the
heart, lung, brain, liver and skeletal muscle of EGF-treated animals.
Changes in Egr-1 levels did not correlate with changes in receptor
phosphorylation or ERK1/2 phosphorylation. In Northern blot analyses,
VEGF induced Egr-1 mRNA levels in all tissues examined except lung and
kidney, whereas EGF led to increased transcripts in all tissues except kidney. In immunofluorescence studies, VEGF induced Egr-1 in
microvascular endothelial cells of the heart and liver, and EGF induced
Egr-1 in the microvascular bed of skeletal muscle. Taken together,
these results suggest that the Egr-1 gene is differentially regulated in response to systemically administered VEGF and EGF.
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