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Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish
During cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges known as trabeculae. Defects in neuregulin signal...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8916774/ https://www.ncbi.nlm.nih.gov/pubmed/35225788 http://dx.doi.org/10.7554/eLife.73231 |
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author | Qi, Jialing Rittershaus, Annegret Priya, Rashmi Mansingh, Shivani Stainier, Didier YR Helker, Christian SM |
author_facet | Qi, Jialing Rittershaus, Annegret Priya, Rashmi Mansingh, Shivani Stainier, Didier YR Helker, Christian SM |
author_sort | Qi, Jialing |
collection | PubMed |
description | During cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges known as trabeculae. Defects in neuregulin signaling, or in endocardial sprouting toward CMs, cause hypotrabeculation. However, the mechanisms underlying endocardial sprouting remain largely unknown. Here, we first show by live imaging in zebrafish embryos that EdCs interact with CMs via dynamic membrane protrusions. After touching CMs, these protrusions remain in close contact with their target despite the vigorous cardiac contractions. Loss of the CM-derived peptide Apelin, or of the Apelin receptor, which is expressed in EdCs, leads to reduced endocardial sprouting and hypotrabeculation. Mechanistically, neuregulin signaling requires endocardial protrusions to induce extracellular signal-regulated kinase (Erk) activity in CMs and trigger their delamination. Altogether, these data show that Apelin signaling-dependent endocardial protrusions modulate CM behavior during trabeculation. |
format | Online Article Text |
id | pubmed-8916774 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-89167742022-03-12 Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish Qi, Jialing Rittershaus, Annegret Priya, Rashmi Mansingh, Shivani Stainier, Didier YR Helker, Christian SM eLife Cell Biology During cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges known as trabeculae. Defects in neuregulin signaling, or in endocardial sprouting toward CMs, cause hypotrabeculation. However, the mechanisms underlying endocardial sprouting remain largely unknown. Here, we first show by live imaging in zebrafish embryos that EdCs interact with CMs via dynamic membrane protrusions. After touching CMs, these protrusions remain in close contact with their target despite the vigorous cardiac contractions. Loss of the CM-derived peptide Apelin, or of the Apelin receptor, which is expressed in EdCs, leads to reduced endocardial sprouting and hypotrabeculation. Mechanistically, neuregulin signaling requires endocardial protrusions to induce extracellular signal-regulated kinase (Erk) activity in CMs and trigger their delamination. Altogether, these data show that Apelin signaling-dependent endocardial protrusions modulate CM behavior during trabeculation. eLife Sciences Publications, Ltd 2022-02-28 /pmc/articles/PMC8916774/ /pubmed/35225788 http://dx.doi.org/10.7554/eLife.73231 Text en © 2022, Qi et al https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Cell Biology Qi, Jialing Rittershaus, Annegret Priya, Rashmi Mansingh, Shivani Stainier, Didier YR Helker, Christian SM Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
title | Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
title_full | Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
title_fullStr | Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
title_full_unstemmed | Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
title_short | Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
title_sort | apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish |
topic | Cell Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8916774/ https://www.ncbi.nlm.nih.gov/pubmed/35225788 http://dx.doi.org/10.7554/eLife.73231 |
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