TSC-22 up-regulates collagen 3a1 gene expression in the rat heart

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http://hdl.handle.net/10138/166646

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Kelloniemi , A , Aro , J , Näpänkangas , J , Koivisto , E , Mustonen , E , Ruskoaho , H & Rysä , J 2015 , ' TSC-22 up-regulates collagen 3a1 gene expression in the rat heart ' , BMC Cardiovascular Disorders , vol. 15 , 122 . https://doi.org/10.1186/s12872-015-0121-2

Title: TSC-22 up-regulates collagen 3a1 gene expression in the rat heart
Author: Kelloniemi, Annina; Aro, Jani; Näpänkangas, Juha; Koivisto, Elina; Mustonen, Erja; Ruskoaho, Heikki; Rysä, Jaana
Other contributor: University of Helsinki, Faculty of Pharmacy



Date: 2015-10-13
Language: eng
Number of pages: 13
Belongs to series: BMC Cardiovascular Disorders
ISSN: 1471-2261
DOI: https://doi.org/10.1186/s12872-015-0121-2
URI: http://hdl.handle.net/10138/166646
Abstract: Background: The transforming growth factor (TGF)-beta is one of the key mediators in cardiac remodelling occurring after myocardial infarction (MI) and in hypertensive heart disease. The TGF-beta-stimulated clone 22 (TSC-22) is a leucine zipper protein expressed in many tissues and possessing various transcription-modulating activities. However, its function in the heart remains unknown. Methods: The aim of the present study was to characterize cardiac TSC-22 expression in vivo in cardiac remodelling and in myocytes in vitro. In addition, we used TSC-22 gene transfer in order to examine the effects of TSC-22 on cardiac gene expression and function. Results: We found that TSC-22 is rapidly up-regulated by multiple hypertrophic stimuli, and in post-MI remodelling both TSC-22 mRNA and protein levels were up-regulated (4.1-fold, P <0.001 and 3.0-fold, P <0.05, respectively) already on day 1. We observed that both losartan and metoprolol treatments reduced left ventricular TSC-22 gene expression. Finally, TSC-22 overexpression by local intramyocardial adenovirus-mediated gene delivery showed that TSC-22 appears to have a role in regulating collagen type III alpha 1 gene expression in the heart. Conclusions: These results demonstrate that TSC-22 expression is induced in response to cardiac overload. Moreover, our data suggests that, by regulating collagen expression in the heart in vivo, TSC-22 could be a potential target for fibrosis-preventing therapies.
Subject: Cardiac hypertrophy
Heart failure
Pressure overload
Myocardial infarction
GROWTH-FACTOR-BETA
ACTIVATED PROTEIN-KINASE
SALIVARY-GLAND CANCER
TGF-BETA
MYOCARDIAL-INFARCTION
STIMULATED CLONE-22
TRANSCRIPTION FACTORS
CARDIAC-HYPERTROPHY
MOLECULAR TARGET
CELL
317 Pharmacy
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