Academic Journal
Arpin deficiency increases actomyosin contractility and vascular permeability
| العنوان: | Arpin deficiency increases actomyosin contractility and vascular permeability |
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| المؤلفون: | Armando Montoya-Garcia, Idaira M Guerrero-Fonseca, Sandra D Chanez-Paredes, Karina B Hernandez-Almaraz, Iliana I Leon-Vega, Angelica Silva-Olivares, Abigail Betanzos, Monica Mondragon-Castelan, Ricardo Mondragon-Flores, Citlaltepetl Salinas-Lara, Hilda Vargas-Robles, Michael Schnoor |
| المصدر: | eLife, Vol 12 (2024) |
| بيانات النشر: | eLife Sciences Publications Ltd, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Medicine LCC:Science LCC:Biology (General) |
| مصطلحات موضوعية: | actin cytoskeleton, vascular permeability, tight junctions, Arp2/3, Medicine, Science, Biology (General), QH301-705.5 |
| الوصف: | 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. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2050-084X |
| Relation: | https://elifesciences.org/articles/90692; https://doaj.org/toc/2050-084X |
| DOI: | 10.7554/eLife.90692 |
| URL الوصول: | https://doaj.org/article/de0546e6962e4806911a827825146387 |
| رقم الانضمام: | edsdoj.0546e6962e4806911a827825146387 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 2050084X |
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| DOI: | 10.7554/eLife.90692 |