Τίτλος:
Thyroid hormone changes cardiomyocyte shape and geometry via ERK signaling pathway: Potential therapeutic implications in reversing cardiac remodeling?
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
It has previously been shown that thyroid hormone can reverse cardiac remodeling in failing hearts by reducing myocardial wall stress due to the unique changes induced in cardiac myocyte shape. This effect may be of therapeutic relevance. Therefore, the present study has investigated potential signaling mechanisms underlying the thyroid hormone action on cardiac myocyte shape and geometry. Neonatal cardiomyocytes were treated with T3 while untreated cells served as controls. T3 administration for 48 h significantly increased the ratio of the major to minor cell axis and changed their shape from an almost circular to an elongated form. Cell area and protein synthesis were increased and T3 treated cells expressed 51% α-MHC and 49% β-MHC as compared to 100% β-MHC expression in non-treated cells. This response was accompanied by a 1.9-fold increase in phospho-ERK levels early at 8 min which, within 60 min, returned to the levels of the untreated cells. Phospho-JNK levels were significantly reduced within 60 min after T3 treatment while no changes in the expression of phospho-Akt and phospho-p38 MAPK were found between the T3 treated and untreated cells. Administration of PD98059 (an inhibitor of ERK signaling) prevented the thyroid hormone induced changes in cardiomyocyte geometry and shape without a significant reduction in cell area and protein synthesis. In conclusion, T3 induced changes in cardiomyocyte shape and geometry involve the ERK kinase signaling. This response is independent of the effects of T3 on cell size and protein synthesis. © Springer Science+Business Media, LLC 2006.
Συγγραφείς:
Pantos, C.
Xinaris, C.
Mourouzis, I.
Malliopoulou, V.
Kardami, E.
Cokkinos, D.V.
Περιοδικό:
Molecular and Cellular Biochemistry
Λέξεις-κλειδιά:
2 (2 amino 3 methoxyphenyl)chromone; liothyronine; major histocompatibility antigen; mitogen activated protein kinase; mitogen activated protein kinase inhibitor; mitogen activated protein kinase p38; protein kinase B; stress activated protein kinase; thyroid hormone, animal cell; antigen expression; article; cell shape; cell size; controlled study; drug potency; geometry; heart failure; heart muscle cell; heart ventricle remodeling; hormone action; newborn; nonhuman; protein phosphorylation; protein synthesis inhibition; rat; signal transduction, Animals; Animals, Newborn; Cell Shape; Cells, Cultured; Electrophoresis, Polyacrylamide Gel; Flavonoids; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase 3; Myocytes, Cardiac; Myosins; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Protein Biosynthesis; Protein Isoforms; Protein Transport; Proto-Oncogene Proteins c-akt; Rats; Triiodothyronine; Ventricular Remodeling
DOI:
10.1007/s11010-006-9323-3
