Endothelial semaphorin 3F maintains endothelial barrier function and inhibits monocyte migration

التفاصيل البيبلوغرافية
العنوان: Endothelial semaphorin 3F maintains endothelial barrier function and inhibits monocyte migration
المؤلفون: Abidemi Junaid, Wendy M.P.J. Sol, Janine M. van Gils, Gangqi Wang, Anton Jan van Zonneveld, Ruben G. de Bruin, Huayu Zhang, Dianne Vreeken
المصدر: International Journal of Molecular Sciences; Volume 21; Issue 4; Pages: 1471
International Journal of Molecular Sciences, 21(4). MDPI
International Journal of Molecular Sciences, Vol 21, Iss 4, p 1471 (2020)
International Journal of Molecular Sciences
سنة النشر: 2020
مصطلحات موضوعية: Nervous system, Angiogenesis, Nerve Tissue Proteins, semaphorin, Article, Catalysis, lcsh:Chemistry, Inorganic Chemistry, Mediator, Immune system, Semaphorin, Human Umbilical Vein Endothelial Cells, medicine, Humans, Physical and Theoretical Chemistry, lcsh:QH301-705.5, Molecular Biology, Spectroscopy, Barrier function, Inflammation, Chemistry, Monocyte, Organic Chemistry, endothelial cells, monocytes, Transendothelial and Transepithelial Migration, Membrane Proteins, General Medicine, Computer Science Applications, Cell biology, HEK293 Cells, medicine.anatomical_structure, lcsh:Biology (General), lcsh:QD1-999, Endothelium, Vascular, Homeostasis
الوصف: In normal physiology, endothelial cells (ECs) form a vital barrier between the blood and underlying tissue controlling leukocyte diapedesis and vascular inflammation. Emerging data suggest that neuronal guidance cues, typically expressed during development, have roles outside the nervous system in vascular biology and immune responses. In particular, Class III semaphorins have been reported to affect EC migration and angiogenesis. While ECs express high levels of semaphorin 3F (SEMA3F), little is known about its function in mature ECs. Here we show that SEMA3F expression is reduced by inflammatory stimuli and increased by laminar flow. Endothelial cells exposed to laminar flow secrete SEMA3F, which subsequently binds to heparan sulfates on the surface of ECs. However, under pro-inflammatory conditions, reduced levels of SEMA3F make ECs more prone to monocyte diapedesis and display impaired barrier function as measured with an electric cell–substrate impedance sensing system and a microfluidic system. In addition, we demonstrate that SEMA3F can directly inhibit the migration of activated monocytes. Taken together, our data suggest an important homeostatic function for EC-expressed SEMA3F, serving as a mediator of endothelial quiescence.
وصف الملف: application/pdf
اللغة: English
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::05053cea0c7da65552fdb1f92e73f570
https://doi.org/10.3390/ijms21041471
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....05053cea0c7da65552fdb1f92e73f570
قاعدة البيانات: OpenAIRE