Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
Vascular tubulogenesis is tightly linked with physiological and pathological events in the living body. Endothelial cells (ECs), which are constantly exposed to hemodynamic forces, play a key role in tubulogenesis. Hydrostatic pressure in particular has been shown to elicit biophysical and biochemical responses leading to EC-mediated tubulogenesis. However, the relationship between tubulogenesis and hydrostatic pressure remains to be elucidated. Here, we propose a specific mechanism through which hydrostatic pressure promotes tubulogenesis. We show that pressure exposure transiently activates the Ras/extracellular signal-regulated kinase (ERK) pathway in ECs, inducing endothelial tubulogenic responses. Water efflux through aquaporin 1 and activation of protein kinase C via specific G protein-coupled receptors are essential to the pressure-induced transient activation of the Ras/ERK pathway. Our approach could provide a basis for elucidating the mechanopathology of tubulogenesis-related diseases and the development of mechanotherapies for improving human health.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:3 |
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| Enthalten in: |
Communications biology - 3(2020), 1 vom: 02. Apr., Seite 152 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Yoshino, Daisuke [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 14.06.2021 Date Revised 14.06.2021 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1038/s42003-020-0881-9 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM308275497 |
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| 100 | 1 | |a Yoshino, Daisuke |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling |
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| 500 | |a Date Revised 14.06.2021 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Vascular tubulogenesis is tightly linked with physiological and pathological events in the living body. Endothelial cells (ECs), which are constantly exposed to hemodynamic forces, play a key role in tubulogenesis. Hydrostatic pressure in particular has been shown to elicit biophysical and biochemical responses leading to EC-mediated tubulogenesis. However, the relationship between tubulogenesis and hydrostatic pressure remains to be elucidated. Here, we propose a specific mechanism through which hydrostatic pressure promotes tubulogenesis. We show that pressure exposure transiently activates the Ras/extracellular signal-regulated kinase (ERK) pathway in ECs, inducing endothelial tubulogenic responses. Water efflux through aquaporin 1 and activation of protein kinase C via specific G protein-coupled receptors are essential to the pressure-induced transient activation of the Ras/ERK pathway. Our approach could provide a basis for elucidating the mechanopathology of tubulogenesis-related diseases and the development of mechanotherapies for improving human health | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Video-Audio Media | |
| 650 | 7 | |a AQP1 protein, human |2 NLM | |
| 650 | 7 | |a Receptors, G-Protein-Coupled |2 NLM | |
| 650 | 7 | |a Water |2 NLM | |
| 650 | 7 | |a 059QF0KO0R |2 NLM | |
| 650 | 7 | |a Aquaporin 1 |2 NLM | |
| 650 | 7 | |a 146410-94-8 |2 NLM | |
| 650 | 7 | |a PRKCA protein, human |2 NLM | |
| 650 | 7 | |a EC 2.7.11.13 |2 NLM | |
| 650 | 7 | |a Protein Kinase C-alpha |2 NLM | |
| 650 | 7 | |a EC 2.7.11.13 |2 NLM | |
| 650 | 7 | |a Extracellular Signal-Regulated MAP Kinases |2 NLM | |
| 650 | 7 | |a EC 2.7.11.24 |2 NLM | |
| 650 | 7 | |a ras Proteins |2 NLM | |
| 650 | 7 | |a EC 3.6.5.2 |2 NLM | |
| 700 | 1 | |a Funamoto, Kenichi |e verfasserin |4 aut | |
| 700 | 1 | |a Sato, Kakeru |e verfasserin |4 aut | |
| 700 | 1 | |a Kenry |e verfasserin |4 aut | |
| 700 | 1 | |a Sato, Masaaki |e verfasserin |4 aut | |
| 700 | 1 | |a Lim, Chwee Teck |e verfasserin |4 aut | |
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