Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis
Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling re...
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| Main Authors: | , , , , , , , , , , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
19 April 2021
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| In: |
Basic research in cardiology
Year: 2021, Volume: 116, Pages: 1-19 |
| ISSN: | 1435-1803 |
| DOI: | 10.1007/s00395-021-00862-y |
| Online Access: | Verlag, kostenfrei, Volltext: https://doi.org/10.1007/s00395-021-00862-y Verlag, kostenfrei, Volltext: https://link.springer.com/10.1007/s00395-021-00862-y 
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| Author Notes: | Gesine M.Dittrich, Natali Froese, Xue Wang, Hannah Kroeger, Honghui Wang, Malgorzata Szaroszyk, Mona Malek-Mohammadi, Julio Cordero, Merve Keles, Mortimer Korf-Klingebiel, Kai C.Wollert, Robert Geffers, Manuel Mayr, Simon J.Conway, Gergana Dobreva, Johann Bauersachs, Joerg Heineke |
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| 245 | 1 | 0 | |a Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis |c Gesine M.Dittrich, Natali Froese, Xue Wang, Hannah Kroeger, Honghui Wang, Malgorzata Szaroszyk, Mona Malek-Mohammadi, Julio Cordero, Merve Keles, Mortimer Korf-Klingebiel, Kai C.Wollert, Robert Geffers, Manuel Mayr, Simon J.Conway, Gergana Dobreva, Johann Bauersachs, Joerg Heineke |
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| 520 | |a Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling remain poorly understood. Cardiac fibroblasts express high levels of cardiogenic transcription factors such as GATA-4 and GATA-6, but their role in fibroblasts during stress is not known. Here, we show that fibroblast GATA-4 and GATA-6 promote adaptive remodeling in pressure overload induced cardiac hypertrophy. Using a mouse model with specific single or double deletion of Gata4 and Gata6 in stress activated fibroblasts, we found a reduced myocardial capillarization in mice with Gata4/6 double deletion following pressure overload, while single deletion of Gata4 or Gata6 had no effect. Importantly, we confirmed the reduced angiogenic response using an in vitro co-culture system with Gata4/6 deleted cardiac fibroblasts and endothelial cells. A comprehensive RNA-sequencing analysis revealed an upregulation of anti-angiogenic genes upon Gata4/6 deletion in fibroblasts, and siRNA mediated downregulation of these genes restored endothelial cell growth. In conclusion, we identified a novel role for the cardiogenic transcription factors GATA-4 and GATA-6 in heart fibroblasts, where both proteins act in concert to promote myocardial capillarization and heart function by directing intercellular crosstalk. | ||
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