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Iranian Journal of Basic Medical Sciences، جلد ۲۳، شماره ۸، صفحات ۱۰۹۱-۱۰۹۹
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عنوان فارسی |
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چکیده فارسی مقاله |
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کلیدواژههای فارسی مقاله |
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عنوان انگلیسی |
Left ventricular phosphorylation patterns of Akt and ERK1/2 after triiodothyronine intracoronary perfusion in isolated hearts and short-term in vivo treatment in Wistar rats |
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چکیده انگلیسی مقاله |
Objective(s): To determine the effects of triiodothyronine (T3) intracoronary perfusion in isolated hearts and short-term administration in rats on the left ventricular (LV) phosphorylation patterns of Akt and ERK1/2. Materials and Methods: Cardiodynamic and hemodynamic parameters were evaluated in Langendorff–perfused hearts. Left ventricles were used for histomorphometric and Western blot analyses. Short-term hyperthyroidism was established by T3 (500 μg.kg-1.d-1; subcutaneous injection) for 1 (T31d), 3 (T33d), and 10 (T310d) days. Results: Isolated hearts receiving T3 perfusion did not modify LV developed pressure, +dP/dtmax, -dP/dtmin, heart rate, and coronary perfusion pressure compared with vehicle-perfused hearts. P-ERK1/2 and p-Akt levels in LV tissues after 5, 15, or 60 min of T3 or vehicle perfusion were similar. Compared with their time-matched controls, isolated hearts of T33d and T310d rats exhibited LV hypertrophy and increased absolute values of +dP/dtmax and -dP/dtmin (i.e., positive inotropic and lusitropic effects). P-ERK1/2 decreased in LV tissues of T31d and T310d but not in those of T33d rats, and p-Akt levels augmented in left ventricles of T33d and stayed unaltered in those of T31d and T310d rats.Conclusion: T3 intracoronary perfusion did not alter cardiodynamics and hemodynamics nor influence the activation of Akt and ERK of normal hearts. Accordingly, the rapid non-genomic effects of T3 were not evident. Short-term T3 treatment provoked cardiac hypertrophy coincidental with increased LV function and associated with transient Akt activation and cyclic ERK1/2 inhibition; which implies activation of physiological hypertrophy signaling and deactivation of pathological hypertrophy signaling, respectively. |
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کلیدواژههای انگلیسی مقاله |
Akt ERK1, 2 Heart hypertrophy Rat Triiodothyronine treatment |
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نویسندگان مقاله |
| Jose Morales Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Ciudad de México, México
| Ruth Lopez Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Ciudad de México, México
| Jorge Lopez Departamento de Biología Celular, Instituto Nacional de Perinatología, Ciudad de México, México
| Jair Lozano Departamento de Biología Celular, Instituto Nacional de Perinatología, Ciudad de México, México
| Rosa Jarillo Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Ciudad de México, México
| Hector Flores Departamento de Inmuno-Bioquímica, Instituto Nacional de Perinatología, Ciudad de México, México
| Enrique Castillo Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Ciudad de México, México
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نشانی اینترنتی |
http://ijbms.mums.ac.ir/article_15831.html |
فایل مقاله |
اشکال در دسترسی به فایل - ./files/site1/rds_journals/87/article-87-2450587.pdf |
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زبان مقاله منتشر شده |
en |
موضوعات مقاله منتشر شده |
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نوع مقاله منتشر شده |
Original Article |
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