ArticleBiology open2021
Tetraspanin18 regulates angiogenesis through VEGFR2 and Notch pathways.
Article in Biology open, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Ononin-modified Chitosan/β-glycerophosphate hydrogel-loaded adipose-derived stem cells promote the repair of diabetic wounds in rats.BMC biotechnology · 2026Article
- GPI transamidase complex is required for primordial germ cell migration and development in zebrafish.Journal of molecular cell biology · 2025Article
- Wound healing and signaling pathways.Open life sciences · 2025Review
- Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury.Advanced healthcare materials · 2023Article
- Angular limb deformity associated with TSPAN18, NRG3 and NOVA2 in Rambouillet rams.Scientific reports · 2023Article
- Sirtuins: Promising Therapeutic Targets to Treat Ischemic Stroke.Biomolecules · 2023Review
- Eugenol attenuates ischemia-mediated oxidative stress in cardiomyocytes via acetylation of histone at H3K27.Free radical biology & medicine · 2023Article
- Notch signalling in healthy and diseased vasculature.Open biology · 2022Review
- Tetraspanin Cd9b plays a role in fertility in zebrafish.PloS one · 2022Article
- A Bioinformatics Perspective on the Links Between Tetraspanin-Enriched Microdomains and Cardiovascular Pathophysiology.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The VEGF pathway is critically required for vasculogenesis, the formation of the primary vascular network. It is also required for angiogenesis resulting in sprouting and pruning of vessels to generate mature arborizing structures. The Notch pathway is essential for arterial-venous specification and the maturation of nascent vessels. We have determined that Tspan18, a member of the Tetraspanin family, is expressed in developing vessels but not in mature vasculature in zebrafish and mouse wound healing. Moreover, reduction at Tspan18 level resulted in aberrant vascular patterning, impaired vessel stability and defective arterial-venous specification. Tspan18 deficiency reduced VEGF, VEGFR2, Notch3 and EphrinB2, and increased EphB4, VEGFR3, Semaphorin3, Neuropilin and PlexinD1 expression. Furthermore, vascular defects of Tspan18 deficiency could be rescued by ectopic expression of VEGFR2 and Notch, but not by knockdown of Semaphorin or Plexin. Functional studies showed that knockdown of Tspan18 led to reduced endothelial cell migration, invasion and tube formation. Tspan18 has dynamic expression, regulates vascular development and maturation in the embryo with re-expression in adult life in wound healing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.