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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Ubiquitin proteasome system (UPS) activation in the cardiac hypertrophy of hyperthyroidism

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Author(s):
Lino, Caroline Antunes [1] ; Demasi, Marilene [2] ; Barreto-Chaves, Maria Luiza [1]
Total Authors: 3
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, Lab Cellular Biol & Funct Anat, Ave Prof Lineu Prestes 2415, BR-05508900 Sao Paulo, SP - Brazil
[2] Butantan Inst, Biochem & Biophys Lab, Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Molecular and Cellular Endocrinology; v. 493, AUG 1 2019.
Web of Science Citations: 1
Abstract

Ubiquitin proteasome system (UPS) is the main proteolytic pathway in eukaryotic cells. Changes in proteasome expression and activity have been associated to cardiovascular diseases as cardiac hypertrophy. Considering that cardiac hypertrophy is commonly associated to hyperthyroidism condition, the present study aimed to investigate the contribution of UPS in cardiac hypertrophy induced by thyroid hormones. Hyperthyroidism was induced in male Wistar rats by intraperitoneal injections of triiodothyronine (T3; 7 mu g/100 g of body weight) for 7 days and confirmed by raised levels of total T3 and decreased levels of total T4. In addition, systolic blood pressure and heart rate were significantly increased in hyperthyroid group. Cardiac hypertrophy was confirmed in hyperthyroid group by increased heart weight/tibia length ratio and by increased alpha-MHC/beta-MHC relative expression. Both catalytic (20SPT) and regulatory subunits (19SPT) of the constitutive proteasome were upregulated in hyperthyroid hearts. In addition, the transcripts that encode immunoproteasome subunits were also elevated. Furthermore, ATP-dependent chymotrypsin-like activity (26SPT) was significantly increased in hyperthyroid group. Despite the upregulation and activation of UPS in hyperthyroid hearts, the content of polyubiquitinated proteins was unaltered in relation to control. Together, these results evidence the activation of cardiac proteasome by thyroid hormones, which possibly contribute to the maintenance of protein quality control and regulation of cardiac hypertrophy in response to thyroid hormones. (AU)

FAPESP's process: 11/01291-3 - THE UBIQUITIN PROTEASOME SYSTEM IN CARDIAC HYPERTROPHY MODEL INDUCED BY THYROID HORMONES.
Grantee:Caroline Antunes Lino
Support type: Scholarships in Brazil - Master