Impaired Ca handling and contraction in cardiomyocytes from mice with a dominant negative thyroid hormone receptor ?

Tavi, Pasi; Sjögren, Maria H.; Lunde, Per; Zhang, Shi‐Jin; Abbate, F.; Vennström, Björn; Westerblad, Håkan

doi:10.1016/j.yjmcc.2005.02.008

Cited by 32 publications

(36 citation statements)

References 127 publications

(159 reference statements)

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“…Upon b-adrenergic stimulation, the mutant cardiomyocytes showed an augmented response, indicating an intact subsequent b-adrenergic signaling cascade; however, the rate of Ca 2? uptake and the relaxation time still remained lower in these cells [25].…”

Section: Cardiac Phenotype Of Tra11m Micementioning

confidence: 81%

“…Compared to the relatively mild bradycardia in vivo, isolated TRa1?m cardiomyocytes exhibited a severe hypothyroid phenotype with impaired contractions, decreased shortening speed, and a prolonged relaxation time [25]. Furthermore, Ca 2?…”

Section: Cardiac Phenotype Of Tra11m Micementioning

confidence: 92%

“…TRa1?m mice show severe abnormalities in several tissues reflecting TRa1-mediated hypothyroidism [14,[24][25][26][27][28]. The animals exhibit lower birth weight and a drastically delayed postnatal development, accompanied by, e.g.…”

Section: Phenotype Of Mice Carrying a Tra1r384c Mutationmentioning

confidence: 99%

“…To understand the consequences of such a defect and to promote the identification of [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29]. The phenotypes of these mutants, which differ substantially depending on the position of the mutation in TRa1, have been summarized in Table 1.…”

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confidence: 99%

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Physiological consequences of the TRα1 aporeceptor state

2008

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Many patients have been characterized harboring a mutation in thyroid hormone receptor (TR) beta. Surprisingly none has yet been identified carrying a mutation in TRalpha1. To facilitate the identification of such patients, several animal models with a mutant TRalpha1 have been generated. While some phenotypic characteristics, such as an adult euthyroidism, are similar in the mutant mice, other aspects such as metabolism are quite variable. This review summarizes the most important consequences of a mutation in TRalpha1 in mice focusing on the TRalpha1-R384C mutation, and projects the insights from the animal models to a putative phenotype of patients with a mutated TRalpha1.

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Section: Cardiac Phenotype Of Tra11m Micementioning

confidence: 81%

Section: Cardiac Phenotype Of Tra11m Micementioning

confidence: 92%

Section: Phenotype Of Mice Carrying a Tra1r384c Mutationmentioning

confidence: 99%

mentioning

confidence: 99%

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Physiological consequences of the TRα1 aporeceptor state

2008

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“…These data probably support the concept that unliganded TRa1 may function as aporeceptor and induce fetal phenotypic changes in cells exposed to prolonged activation of a1-adrenergic signaling. This notion is further supported by the fact that overexpression of unliganded TRa1 receptor in neonatal cardiomyocytes resulted in cell growth with fetal pattern of myosin isoform expression [13] and cardiomyocytes from mice with dominant negative TRa1 displayed impaired calcium handling and contraction [14]. Here, it should be noted that TRa1 appears also to be critical in the differentiation of cardiac embryonic cells [12].…”

Section: Introductionmentioning

confidence: 94%

Rebuilding the post-infarcted myocardium by activating ‘physiologic’ hypertrophic signaling pathways: the thyroid hormone paradigm

2008

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Viable myocardium undergoes several changes in the course of cardiac remodeling following myocardial infarction aiming to adapt the heart to the hemodynamic compromise. This response is characterized by reactivation of the fetal transcriptional program and results in cardiac dysfunction. Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can "rebuild" the post-infarcted heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac chamber geometry. This effect seems to be attributed to TH pleiotropic cellular actions; TH promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival upon stress. TH may constitute a new therapeutic option for mending the ischemic myocardium.

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