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J. Biol. Chem., Vol. 278, Issue 17, 15073-15083, April 25, 2003
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From the Brain natriuretic peptide (BNP) gene expression
is a well documented marker of hypertrophy in the cardiac myocyte.
Triiodothyronine (T3), the bioactive form of thyroid
hormone, triggers a unique form of hypertrophy in cardiac myocytes that
accompanies the selective activation or suppression of specific gene
targets. In this study, we show that the BNP gene is a target of
T3 action. BNP secretion was increased 6-fold, BNP mRNA
levels 3-fold, and BNP promoter activity 3-5-fold following
T3 treatment. This was accompanied by an increase in
myocyte size, sarcomeric organization, and protein synthesis. Of note,
several of the responses to T3 synergized with those to the
conventional hypertrophic agonist endothelin. The response to the
liganded thyroid hormone receptor (TR) was mediated by an unusual
thyroid hormone response element located between
Triiodothyronine Increases Brain Natriuretic Peptide
(BNP) Gene Transcription and Amplifies
Endothelin-dependent BNP Gene Transcription and
Hypertrophy in Neonatal Rat Ventricular Myocytes*
,,,, and§¶
Diabetes Center/Metabolic Research Unit and
the § Department of Medicine, University of California,
San Francisco, California 94143-0540
1000 and 987
relative to the transcription start site. Both TR homodimers and
TR·retinoid X receptor heterodimers associated with this element in an electrophoretic mobility shift assay. Protein fragments harboring the LXXLL motifs of the
coactivators GRIP1 and SRC1 or TRAP220 interacted predominantly with
the TR·retinoid X receptor heterodimeric pair in a
ligand-dependent fashion. Both TR homodimers and
heterodimers in the unliganded state selectively associated with
glutathione S-transferase-nuclear receptor corepressor fragments harboring one of three receptor interaction domains containing the sequence (I/L)XX(I/V)I. These
interactions were dissociated following the addition of T3.
Collectively, these findings identify the BNP gene as a potential model
for the investigation of TR-dependent gene regulation in
the heart.
*
This work was supported by National Institutes of Health
Grant HL35753 and American Heart Association Grant 9950062N.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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