help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wu, P. S.-C.
Right arrow Articles by Dillmann, W. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wu, P. S.-C.
Right arrow Articles by Dillmann, W. H.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*LIOTHYRONINE
Endocrinology Vol. 138, No. 1 114-120
Copyright © 1997 by The Endocrine Society

ARTICLES

{alpha}1-Adrenergic Stimulation Inhibits 3,5,3'-Triiodothyronine-Induced Expression of the Rat Heart Sarcoplasmic Reticulum Ca2+ Adenosine Triphosphatase Gene1

Patricia S.-C. Wu, Anselmo S. Moriscot, Kirk U. Knowlton, Randa Hilal-Dandan, Huaping He and Wolfgang H. Dillmann

Department of Medicine, Divisions of Endocrinology (P.S.W., A.S.M., H.H., W.H.D.), Cardiology (K.U.K.), and Pharmacology (R.H.-D.), University of California-San Diego, La Jolla, California 92093-0618

Address all correspondence and requests for reprints to: Wolfgang H. Dillmann, M.D., Department of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, California 92093-0618.

The interactions between the ß-adrenergic system and thyroid hormone (T3) on cardiac function have been investigated in detail. In addition to ß-adrenoceptors, {alpha}1-adrenergic receptors are present in the mammalian heart. The interactions between T3 and the {alpha}1-adrenergic system remain, however, poorly understood. T3 stimulates the expression and transcription of the sarcoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA2) gene, a protein vital in the control of cardiac calcium transients and contractility. We show that in rat cardiac myocytes, the stimulatory effect of T3 on SERCA2 messenger RNA expression and gene transcription is inhibited by an {alpha}1-adrenergic agonist. We demonstrate that direct activation of the {alpha}1-adrenergic signaling pathway, using a mutant constitutively active G protein (Gq) similarly down-regulated the T3 effect on SERCA2 transcription. The combined effect of thyroid hormone receptor and retinoid X receptors on T3-stimulated SERCA2 gene transcription was also markedly attenuated by {alpha}1-adrenergic stimulation. These results suggested that activation of the {alpha}1-adrenergic signaling pathway has an inhibitory effect on T3-dependent SERCA2 gene transcription. As this inhibitory effect of {alpha}1-adrenergic stimulation occurs when only one thyroid hormone response element (TRE) drives reporter expression, it is most likely mediated by an alteration of the nuclear factors binding to the TRE or by influencing the interaction of the TRE complex with the basal transcriptional machinery.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. Hilal-Dandan, H. He, J. L. Martin, L. L. Brunton, and W. H. Dillmann
Endothelin downregulates SERCA2 gene and protein expression in adult rat ventricular myocytes: regulation by pertussis toxin-sensitive Gi protein and cAMP
Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H728 - H734.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
G. J. Kahaly and W. H. Dillmann
Thyroid Hormone Action in the Heart
Endocr. Rev., August 1, 2005; 26(5): 704 - 728.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
P. D. Ho, J.-S. Fan, N. L. Hayes, N. Saada, P. T. Palade, C. C. Glembotski, and P. M. McDonough
Ras Reduces L-Type Calcium Channel Current in Cardiac Myocytes : Corrective Effects of L-Channels and SERCA2 on [Ca2+]i Regulation and Cell Morphology
Circ. Res., January 19, 2001; 88(1): 63 - 69.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
B. Gloss, S. Villegas, F. J. Villarreal, A. Moriscot, and W. H. Dillmann
Thyroid hormone-induced stimulation of the sarcoplasmic reticulum Ca2+ ATPase gene is inhibited by LIF and IL-6
Am J Physiol Endocrinol Metab, April 1, 2000; 278(4): E738 - E743.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
R. E. Weiss, Y. Murata, K. Cua, Y. Hayashi, H. Seo, and S. Refetoff
Thyroid Hormone Action on Liver, Heart, and Energy Expenditure in Thyroid Hormone Receptor {beta}-Deficient Mice
Endocrinology, December 1, 1998; 139(12): 4945 - 4952.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
P. D. Ho, D. K. Zechner, H. He, W. H. Dillmann, C. C. Glembotski, and P. M. McDonough
The Raf-MEK-ERK Cascade Represents a Common Pathway for Alteration of Intracellular Calcium by Ras and Protein Kinase C in Cardiac Myocytes
J. Biol. Chem., August 21, 1998; 273(34): 21730 - 21735.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1997 by The Endocrine Society