Left-Ventricular Remodeling After Myocardial Infarction Is Associated with a Cardiomyocyte-Specific Hypothyroid Condition

被引:83
作者
Pol, Christine J. [1 ]
Muller, Alice [1 ]
Zuidwijk, Marian J. [1 ]
van Deel, Elza D. [2 ]
Kaptein, Ellen [3 ]
Saba, Alessandro [4 ]
Marchini, Maja [5 ]
Zucchi, Riccardo [5 ]
Visser, Theo J. [3 ]
Paulus, Walter J. [1 ]
Duncker, Dirk J. [2 ]
Simonides, Warner S. [1 ]
机构
[1] Vrije Univ Amsterdam, Inst Cardiovasc Res, Physiol Lab, Univ Med Ctr, NL-1081 HV Amsterdam, Netherlands
[2] Erasmus Univ, Med Ctr, Thoraxctr, NL-3015 CE Rotterdam, Netherlands
[3] Erasmus Univ, Med Ctr, Dept Internal Med, NL-3015 CE Rotterdam, Netherlands
[4] Univ Pisa, Dipartimento Chim & Chim Ind, I-56126 Pisa, Italy
[5] Univ Pisa, Dipartimento Sci Uomo & Ambiente, I-56126 Pisa, Italy
关键词
TYPE-3 IODOTHYRONINE DEIODINASE; CONGESTIVE-HEART-FAILURE; CARDIAC GENE-EXPRESSION; MYOSIN HEAVY-CHAIN; GROWTH-FACTOR-BETA; THYROID-HORMONE; MOLECULAR-BASIS; HYPERTROPHY; DYSFUNCTION; INDUCTION;
D O I
10.1210/en.2010-0431
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Similarities in cardiac gene expression in hypothyroidism and left ventricular (LV) pathological remodeling after myocardial infarction (MI) suggest a role for impaired cardiac thyroid hormone (TH) signaling in the development of heart failure. Increased ventricular activity of the TH-degrading enzyme type 3 deiodinase (D3) is recognized as a potential cause. In the present study, we investigated the cardiac expression and activity of D3 over an 8-wk period after MI in C57Bl/6J mice. Pathological remodeling of the noninfarcted part of the LV was evident from cardiomyocyte hypertrophy, interstitial fibrosis, and impairment of contractility. These changes were maximal and stable from the first week onward, as was the degree of LV dilation. A strong induction of D3 activity was found, which was similarly stable for the period examined. Plasma T-4 levels were transiently decreased at 1 wk after MI, but T-3 levels remained normal. The high D3 activity was associated with increased D3 mRNA expression at 1 but not at 4 and 8 wk after MI. Immunohistochemistry localized D3 protein to cardiomyocytes. In vivo measurement of TH-dependent transcription activity in cardiomyocytes using a luciferase reporter assay indicated a 48% decrease in post-MI mice relative to sham-operated animals, and this was associated with a 50% decrease in LVtissue T-3 concentration. In conclusion, pathological ventricular remodeling after MIin the mouse leads to high and stable induction of D3 activity in cardiomyocytes and a local hypothyroid condition. (Endocrinology 152: 669-679, 2011)
引用
收藏
页码:669 / 679
页数:11
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