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Myocardial Type III Deiodinase Expression, Protein, and T3 Concentrations in Human Heart Failure
Author(s) -
McElligott Andrew,
Chu Miensheng,
Patel Nilam,
Paul Jennifer T,
Henderson Kyle K
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1040.6
Subject(s) - heart failure , deiodinase , medicine , dilated cardiomyopathy , ischemic cardiomyopathy , triiodothyronine , cardiomyopathy , endocrinology , cardiology , ventricular remodeling , chemistry , ejection fraction , hormone
Recent studies demonstrate type III deiodinase (D3) activity is increased in animal models of heart failure. D3 is a fetal enzyme which inactivates triiodothyronine (T3) which may contribute to left ventricular remodeling by altering T3 dependent gene expression and cell signaling. We hypothesized myocardial D3 expression and protein levels would be increased in heart failure patients and result in lower myocardial T3 concentrations. Left ventricular D3 expression levels in heart failure patients with dilated (DCM; 1.6±0.4; N=17) or ischemic cardiomyopathy (ICM; 1.1±0.3; N=9), were not different than “non‐failing” samples obtained from the Gift of Hope (GOH; 1.0±0.2 RQ; N=16). Similarly, D3 protein levels were not different: DCM (0.10±0.02; N=28), ICM (0.09±0.02; N=17) vs. GOH (0.10±0.01 D3/actin OD; N=11). Preliminary myocardial T3 concentration data suggest no difference between DCM (1.1±0.2; N=3) and GOH (1.1±0.1ng/g; N=3). Serum T3 concentrations were also similar: DCM (92.6±10.4; N=10), ICM (98.7; N=1), and GOH (84.9±13.7ng/dL; N=11). Importantly, serum T3 concentrations in 10 healthy controls were greater (170.9±5.7ng/dL; P<0.05). These data suggest failing and “non‐failing” human myocardial tissue may have low T3 concentrations which could alter left ventricular function and remodeling. Funding: Falk Medical Research Trust and Stritch School of Medicine Research Funding Committee.