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Title of Journal: Cell Tissue Res

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Abbravation: Cell and Tissue Research

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Publisher

Springer Berlin Heidelberg

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DOI

10.1007/bf01732243

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ISSN

1432-0878

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Transcription factor PEX1 modulates extracellular

Authors: Alicia Jurado Acosta Jaana Rysä Zoltan Szabo AnneMari Moilanen Hiba Komati Mona Nemer Heikki Ruskoaho
Publish Date: 2016/11/08
Volume: 367, Issue: 2, Pages: 369-385
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Abstract

The phenylephrineinduced complex1 PEX1 transcription factor also known as zincfinger protein 260 Zfp260 is an effector of endothelin1 and α1adrenergic signaling in cardiac hypertrophy However the role of PEX1 in transcriptional regulation of myocardial remodeling remains largely unknown In the present study we used PEX1 gain and lossoffunction to examine the effects of PEX1 on left ventricular remodeling Adenoviral constructs expressing PEX1 antisense PEX1 or LacZ were delivered by local injection into the anterior wall of the left ventricle in Sprague–Dawley rats PEX1 overexpression led to induction of hypertrophic gene program and increased fibrosis In agreement with this the expression of genes involved in the fibrotic process such as collagens I and III matrix metalloproteinases MMPs fibronectin1 transforming growth factor beta1 and connective tissue growth factor were significantly upregulated following PEX1 overexpression whereas silencing of PEX1 significantly inhibited the expression of profibrotic genes and increased left ventricular ejection fraction and fractional shortening In vitro luciferase reporter assays showed that PEX1 regulates the expression of MMP9 by activating promoter Furthermore PEX1 gain and lossoffunction experiments in rat neonatal cardiac fibroblasts and myocytes revealed that MMP9 gene expression was affected by PEX1 predominantly in fibroblasts Our results indicate that PEX1 is involved in regulating cardiac fibrosis and extracellular matrix turnover particularly fibroblasts being responsible for the fibrosisassociated changes in gene expression Furthermore PEX1 activation of the MMP9 promoter triggers the profibrotic response directed by PEX1We thank Professor Wolfgang Eberhardt Pharmazentrum Frankfurt/ZAFES Klinikum der GoetheUniversität Frankfurt Frankfurt am Main Germany for the pGLIIIpMMP9Luc construct and Professor Olli Vuolteenaho Research Unit of Biomedicine University of Oulu Finland for kindly providing Ang II We also thank Marja Arbelius Kati Lampinen Kirsi Salo and Sirpa Rutanen for their expert technical assistance This work was supported by the Finnish Foundation for Cardiovascular Research to AJA HR ZS the Sigrid Jusélius Foundation to HR the Academy of Finland grants 266661 to HR and 276747 to JR and the Heart and Stroke Foundation of Canada grant NA7301 to HK and MN

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