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Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution
To create a closed vascular system, angiogenic sprouts must meet and connect in a process called vessel fusion, which is a prerequisite for establishment of proper blood flow in nascent vessels. However, the molecular machinery underlying this process remains largely unknown. Herein, we report that...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489673/ https://www.ncbi.nlm.nih.gov/pubmed/34766111 http://dx.doi.org/10.1002/mco2.9 |
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author | Kong, Lingmiao Xiao, Fei Wang, Lijun Li, Min Wang, Denian Feng, Zhongxue Huang, Luping Wei, Yong'gang Li, Hongyu Liu, Fei Kang, Yan Liao, Xuelian Zhang, Wei |
author_facet | Kong, Lingmiao Xiao, Fei Wang, Lijun Li, Min Wang, Denian Feng, Zhongxue Huang, Luping Wei, Yong'gang Li, Hongyu Liu, Fei Kang, Yan Liao, Xuelian Zhang, Wei |
author_sort | Kong, Lingmiao |
collection | PubMed |
description | To create a closed vascular system, angiogenic sprouts must meet and connect in a process called vessel fusion, which is a prerequisite for establishment of proper blood flow in nascent vessels. However, the molecular machinery underlying this process remains largely unknown. Herein, we report that intermedin (IMD), a calcitonin family member, promotes vessel fusion by inducing endothelial cells (ECs) to enter a “ready‐to‐anchor” state. IMD promotes vascular endothelial cadherin (VEC) accumulation at the potential fusion site to facilitate anchoring of approaching vessels to each other. Simultaneously, IMD fine‐tunes VEC activity to achieve a dynamic balance between VEC complex dissociation and reconstitution in order to widen the anastomotic point. IMD induces persistent VEC phosphorylation. Internalized phospho‐VEC preferentially binds to Rab4 and Rab11, which facilitate VEC vesicle recycling back to the cell‐cell contact for reconstruction of the VEC complex. This novel mechanism may explain how neovessels contact and fuse to adjacent vessels to create a closed vascular system. |
format | Online Article Text |
id | pubmed-8489673 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84896732021-11-10 Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution Kong, Lingmiao Xiao, Fei Wang, Lijun Li, Min Wang, Denian Feng, Zhongxue Huang, Luping Wei, Yong'gang Li, Hongyu Liu, Fei Kang, Yan Liao, Xuelian Zhang, Wei MedComm (2020) Original Articles To create a closed vascular system, angiogenic sprouts must meet and connect in a process called vessel fusion, which is a prerequisite for establishment of proper blood flow in nascent vessels. However, the molecular machinery underlying this process remains largely unknown. Herein, we report that intermedin (IMD), a calcitonin family member, promotes vessel fusion by inducing endothelial cells (ECs) to enter a “ready‐to‐anchor” state. IMD promotes vascular endothelial cadherin (VEC) accumulation at the potential fusion site to facilitate anchoring of approaching vessels to each other. Simultaneously, IMD fine‐tunes VEC activity to achieve a dynamic balance between VEC complex dissociation and reconstitution in order to widen the anastomotic point. IMD induces persistent VEC phosphorylation. Internalized phospho‐VEC preferentially binds to Rab4 and Rab11, which facilitate VEC vesicle recycling back to the cell‐cell contact for reconstruction of the VEC complex. This novel mechanism may explain how neovessels contact and fuse to adjacent vessels to create a closed vascular system. John Wiley and Sons Inc. 2020-06-09 /pmc/articles/PMC8489673/ /pubmed/34766111 http://dx.doi.org/10.1002/mco2.9 Text en © 2020 The Authors. MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Kong, Lingmiao Xiao, Fei Wang, Lijun Li, Min Wang, Denian Feng, Zhongxue Huang, Luping Wei, Yong'gang Li, Hongyu Liu, Fei Kang, Yan Liao, Xuelian Zhang, Wei Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution |
title | Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution |
title_full | Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution |
title_fullStr | Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution |
title_full_unstemmed | Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution |
title_short | Intermedin promotes vessel fusion by inducing VE‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between VE‐cadherin‐complex dissociation/reconstitution |
title_sort | intermedin promotes vessel fusion by inducing ve‐cadherin accumulation at potential fusion sites and to achieve a dynamic balance between ve‐cadherin‐complex dissociation/reconstitution |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489673/ https://www.ncbi.nlm.nih.gov/pubmed/34766111 http://dx.doi.org/10.1002/mco2.9 |
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