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Vol. 57, Issue 5, 984-990, May 2000
1-Adrenergic Stimulation of Fibroblast Growth Factor-2
Promoter Activity in Cardiac Myocytes
Gene Technology and Departments of Physiology, and Pharmacology and
Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada
Fibroblast growth factor-2 (FGF-2), a mitogenic, angiogenic, and
cardioprotective agent, is released from the postnatal heart by a
mechanism of transient remodelling of the sarcolemma during contraction. Both release of FGF-2 and its synthesis can be increased with adrenergic stimulation. We reported previously that FGF-2 synthesis can be regulated at the transcriptional level by
-adrenergic stimulation of cultured neonatal rat
cardiac myocytes as well as in the adult mouse heart. Examination of
the proximal promoter region of both human and rat FGF-2 gene sequences
revealed binding sites for the early growth response-1 (Egr-1) protein.
Using gel mobility shift assays, we observed a transient increase in a
complex between nuclear extracts from neonatal rat cardiac myocytes
treated with inducers of Egr-1, including the
-adrenergic agonist phenylephrine, angiotensin II,
and phorbol ester, and a consensus Egr-1 DNA element. A similar complex
was seen with the FGF-2 promoter region 
7/+42 as the DNA probe, but
not when the Egr-1 element at nucleotides +3/+31 was disrupted.
Participation of Egr-1 protein in the complex was confirmed by
competition with Egr-1 DNA elements and antibodies. With deletion
analysis and transfection of neonatal rat cardiac myocytes, the
-adrenergic response was localized to nucleotides 110/+42 of the FGF-2 gene in the context of a hybrid FGF-2/luciferase reporter gene, 110FGFp.luc. Overexpression of Egr-1
increased 110FGFp.luc gene expression, whereas
mutation of its Egr-1 element at nucleotides +3/+31 abolished
-adrenergic responsiveness. These data indicate that
Egr-1 is involved in the -adrenergic stimulation of
the FGF-2 promoter region in neonatal cardiac myocytes.
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