ArticleMolecular and cellular biochemistry2010
Non-genomic effects of thyroid hormone in adult cardiac myocytes: relevance to gene expression and cell growth.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 36 citations in OpenAlex.
- Cardiac hypertrophy that affects hyperthyroidism occurs independently of the NLRP3 inflammasome.Pflugers Archiv : European journal of physiology · 2024Article
- The Intrinsic Activity of Thyroxine Is Critical for Survival and Growth and Regulates Gene Expression in Neonatal Liver.Thyroid : official journal of the American Thyroid Association · 2021Article
- Topical L-thyroxine: The Cinderella among hormones waiting to dance on the floor of dermatological therapy?Experimental dermatology · 2020Review
- Left ventricular phosphorylation patterns of Akt and ERK1/2 after triiodothyronine intracoronary perfusion in isolated hearts and short-termIranian journal of basic medical sciences · 2020Article
- Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism.International journal of molecular sciences · 2020Review
- Thyroid hormone receptor function in maturing ovine cardiomyocytes.The Journal of physiology · 2019Article
- Thyroid states regulate subcellular glucose phosphorylation activity in male mice.Endocrine connections · 2017Article
- S100A8/MYD88/NF-қB: a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Repair Injured Heart by Regulating Cardiac Regenerative Signals.Stem cells international · 2016Review
- Thyroid hormone promotes insulin-induced glucose uptake by enhancing Akt phosphorylation and VAMP2 translocation in 3T3-L1 adipocytes.Journal of cellular physiology · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Besides the well-characterized genomic action of thyroid hormone (TH), mediated by thyroid hormone receptors (TRs), accumulating data support the so-called non-genomic action of TH, which is often related to activation of signalling pathways. In this study, we sought to determine whether TH activates intracellular signalling pathways in the adult cardiac myocytes and whether such activation modulates cell growth and the expression of target proteins important in cardiac function. We demonstrate that TH promotes a rapid increase in the phosphorylation of several kinases, ERK1/2, PKCdelta, p38-MAPK and Akt. This activation is inhibited by triiodothyroacetic acid (triac), which is a TH analogue known to displace the hormone from membrane bound receptors, indicating that this TH effect is mediated through a cell membrane-initiated mechanism. Furthermore, using specific inhibitors of the TH-activated kinases, we show that the long-term effects of TH on the expression of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA), alpha- and beta-myosin heavy chain (MHC) and cell growth are reverted, implying that what is initiated as a non-genomic action of the hormone interfaces with genomic effects. These data provide further insights into the underlying mechanisms of TH action in the heart with potentially important implications in the management of cardiac pathology.
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