Endothelial β‐arrestins regulate mechanotransduction by the type II bone morphogenetic protein receptor in primary cilia Article Swipe
Saejeong Park
,
Zhiyuan Ma
,
Georgia Zarkada
,
Irinna Papangeli
,
Sarin N Paluri
,
Nour Nazo
,
Félix Rivera-Molina
,
Derek Toomre
,
Sudarshan Rajagopal
,
Hyung J. Chun
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1002/pul2.12167
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1002/pul2.12167
Modulation of endothelial cell behavior and phenotype by hemodynamic forces involves many signaling components, including cell surface receptors, intracellular signaling intermediaries, transcription factors, and epigenetic elements. Many of the signaling mechanisms that underlie mechanotransduction by endothelial cells are inadequately defined. Here we sought to better understand how β‐arrestins, intracellular proteins that regulate agonist‐mediated desensitization and integration of signaling by transmembrane receptors, may be involved in the endothelial cell response to shear stress. We performed both in vitro studies with primary endothelial cells subjected to β‐arrestin knockdown, and in vivo studies using mice with endothelial specific deletion of β‐arrestin 1 and β‐arrestin 2. We found that β‐arrestins are localized to primary cilia in endothelial cells, which are present in subpopulations of endothelial cells in relatively low shear states. Recruitment of β‐arrestins to cilia involved its interaction with IFT81, a component of the flagellar transport protein complex in the cilia. β‐arrestin knockdown led to marked reduction in shear stress response, including induction of NOS3 expression. Within the cilia, β‐arrestins were found to associate with the type II bone morphogenetic protein receptor (BMPR‐II), whose disruption similarly led to an impaired endothelial shear response. β‐arrestins also regulated Smad transcription factor phosphorylation by BMPR‐II. Mice with endothelial specific deletion of β‐arrestin 1 and β‐arrestin 2 were found to have impaired retinal angiogenesis. In conclusion, we have identified a novel role for endothelial β‐arrestins as key transducers of ciliary mechanotransduction that play a central role in shear signaling by BMPR‐II and contribute to vascular development.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/pul2.12167
- https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/pul2.12167
- OA Status
- gold
- Cited By
- 6
- References
- 53
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4311211728
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4311211728Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1002/pul2.12167Digital Object Identifier
- Title
-
Endothelial β‐arrestins regulate mechanotransduction by the type II bone morphogenetic protein receptor in primary ciliaWork title
- Type
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articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-10-01Full publication date if available
- Authors
-
Saejeong Park, Zhiyuan Ma, Georgia Zarkada, Irinna Papangeli, Sarin N Paluri, Nour Nazo, Félix Rivera-Molina, Derek Toomre, Sudarshan Rajagopal, Hyung J. ChunList of authors in order
- Landing page
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https://doi.org/10.1002/pul2.12167Publisher landing page
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/pul2.12167Direct link to full text PDF
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/pul2.12167Direct OA link when available
- Concepts
-
Cell biology, Mechanotransduction, Arrestin, Endothelial stem cell, Bone morphogenetic protein, Angiogenesis, Signal transduction, Biology, G protein-coupled receptor, Cancer research, Gene, In vitro, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
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6Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 1, 2024: 4, 2022: 1Per-year citation counts (last 5 years)
- References (count)
-
53Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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