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Adenoviral constructs overexpressing wild\u2010type GATA4 or GATA4 mutated at S105 were delivered into the anterior LV free wall. AngII (33.3\u00a0\u00b5g\/kg\/h) was administered via subcutaneously implanted minipumps. Cardiac function and structure were examined by echocardiography, followed by histological immunostainings of LV sections and gene expression measurements by RT\u2010qPCR. The effects of GATA4 on cultured neonatal rat ventricular fibroblasts were evaluated. In AngII\u2010induced hypertension, GATA4 overexpression repressed fibrotic gene expression, reversed the hypertrophic adult\u2010to\u2010foetal isoform switch of myofibrillar genes and prevented apoptosis, whereas histological fibrosis was not affected. Overexpression of GATA4 mutated at S105 resulted in LV chamber dilatation, cardiac dysfunction and had minor effects on expression of myocardial remodelling genes. Fibrotic gene expression in cardiac fibroblasts was differently affected by overexpression of wild\u2010type or mutated GATA4. Our results indicate that GATA4 reduces AngII\u2010induced responses by interfering with pro\u2010fibrotic and hypertrophic gene expressions. GATA4 actions on LV remodelling and fibroblasts are dependent on phosphorylation site S105.<\/jats:p>","DOI":"10.1111\/bcpt.13398","type":"journal-article","created":{"date-parts":[[2020,2,15]],"date-time":"2020-02-15T08:54:19Z","timestamp":1581756859000},"page":"178-195","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Phosphorylation of GATA4 at serine 105 is required for left ventricular remodelling process in angiotensin II\u2010induced hypertension in rats"],"prefix":"10.1111","volume":"127","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3679-8395","authenticated-orcid":false,"given":"Alicia","family":"Jurado Acosta","sequence":"first","affiliation":[{"name":"Pharmacology and Toxicology Biomedicine Research Unit Faculty of Medicine University of Oulu Oulu 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