Arpin deficiency increases actomyosin contractility and vascular permeability Article Swipe
Armando Montoya‐García
,
Idaira M. Guerrero-Fonseca
,
Sandra D. Chánez-Paredes
,
Karina B. Hernández-Almaraz
,
Iliana I. León-Vega
,
Angélica Silva-Olivares
,
Abigail Betanzos
,
Mónica Mondragón‐Castelán
,
Ricardo Mondragón‐Flores
,
Citlaltepetl Salinas‐Lara
,
Hilda Vargas‐Robles
,
Michael Schnoor
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.7554/elife.90692
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.7554/elife.90692
Arpin was discovered as an inhibitor of the Arp2/3 complex localized at the lamellipodial tip of fibroblasts, where it regulated migration steering. Recently, we showed that arpin stabilizes the epithelial barrier in an Arp2/3-dependent manner. However, the expression and functions of arpin in endothelial cells (EC) have not yet been described. Arpin mRNA and protein are expressed in EC and downregulated by pro-inflammatory cytokines. Arpin depletion in Human Umbilical Vein Endothelial Cells causes the formation of actomyosin stress fibers leading to increased permeability in an Arp2/3-independent manner. Instead, inhibitors of ROCK1 and ZIPK, kinases involved in the generation of stress fibers, normalize the loss-of-arpin effects on actin filaments and permeability. Arpin-deficient mice are viable but show a characteristic vascular phenotype in the lung including edema, microhemorrhage, and vascular congestion, increased F-actin levels, and vascular permeability. Our data show that, apart from being an Arp2/3 inhibitor, arpin is also a regulator of actomyosin contractility and endothelial barrier integrity.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.7554/elife.90692
- OA Status
- gold
- Cited By
- 2
- References
- 44
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4387136573
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4387136573Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.7554/elife.90692Digital Object Identifier
- Title
-
Arpin deficiency increases actomyosin contractility and vascular permeabilityWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-09-28Full publication date if available
- Authors
-
Armando Montoya‐García, Idaira M. Guerrero-Fonseca, Sandra D. Chánez-Paredes, Karina B. Hernández-Almaraz, Iliana I. León-Vega, Angélica Silva-Olivares, Abigail Betanzos, Mónica Mondragón‐Castelán, Ricardo Mondragón‐Flores, Citlaltepetl Salinas‐Lara, Hilda Vargas‐Robles, Michael SchnoorList of authors in order
- Landing page
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https://doi.org/10.7554/elife.90692Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.7554/elife.90692Direct OA link when available
- Concepts
-
Cell biology, Actin, Contractility, Stress fiber, Vascular permeability, Biology, Regulator, ROCK1, Permeability (electromagnetism), Chemistry, RHOA, Focal adhesion, Phosphorylation, Signal transduction, Biochemistry, Endocrinology, Gene, MembraneTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
2Total citation count in OpenAlex
- Citations by year (recent)
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2025: 2Per-year citation counts (last 5 years)
- References (count)
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44Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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