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MiRNA-208a and miRNA-208b are triggered in thyroid hormone-induced cardiac hypertrophy - role of type 1 Angiotensin II receptor (AT1R) on miRNA-208a/α-MHC modulation
- Source :
- Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual), Universidade de São Paulo (USP), instacron:USP
- Publication Year :
- 2012
-
Abstract
- Hyperthyroidism promotes cardiac hypertrophy and the Angiotensin type 1 receptor (AT1R) has been demonstrated to mediate part of this response. Recent studies have uncovered a potentially important role for the microRNAs (miRNAs) in the control of diverse aspects of cardiac function. Then, the objective of the present study was to investigate the action promoted by hyperthyroidism on β-MHC/miR-208b expression and on α-MHC/miR-208a expression, as well as the possible contribution of the AT1R in this event. The findings of this study confirmed that AT1R is a key mediator of the cardiac hypertrophy induced by hyperthyroidism. Additionally, we demonstrated that like β-MHC, miR-208b was down-regulated in the hyperthyroid group. Similarly, like the expression of its host gene, α-MHC, miR-208a expression was up-regulated in response to hyperthyroidism. Finally, our data suggest for the first time that AT1R mediates the hyperthyroidism-induced increase on cardiac miRNA-208a/α-MHC levels, while does not influence on the reduction of miRNA-208b/β-MHC levels.
- Subjects :
- Cardiac function curve
Male
endocrine system
Angiotensin receptor
medicine.medical_specialty
Thyroid Hormones
endocrine system diseases
Primary Cell Culture
Thyroid Gland
Cardiomegaly
Biology
Biochemistry
Hyperthyroidism
Receptor, Angiotensin, Type 1
Endocrinology
Mediator
Internal medicine
medicine
Animals
Myocytes, Cardiac
Rats, Wistar
Receptor
Molecular Biology
Regulation of gene expression
Angiotensin II receptor type 1
Myosin Heavy Chains
ANATOMIA
Rats
MicroRNAs
Animals, Newborn
Gene Expression Regulation
MYH6
Signal transduction
Signal Transduction
Subjects
Details
- ISSN :
- 18728057
- Volume :
- 374
- Issue :
- 1-2
- Database :
- OpenAIRE
- Journal :
- Molecular and cellular endocrinology
- Accession number :
- edsair.doi.dedup.....934eb1a45bccf19b3a7fd21befdfca96