ArticleCell communication and signaling : CCS2019
The small GTPase Rab5c is a key regulator of trafficking of the CD93/Multimerin-2/β1 integrin complex in endothelial cell adhesion and migration.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07035249 (A Prospective, Single-Arm Clinical Trial Evaluating DCSZ11 Combined With Standard-of-Care Therapy in Patients With Advanced or Metastatic Solid Tumors), which is not on this map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Prospective, Single-Arm Clinical Trial Evaluating DCSZ11 Combined With Standard-of-Care Therapy in Patients With Advanced or Metastatic Solid Tumors
Who cites it
27 citing papers in PubMed.
- Behind the scenes: how the EMILIN/Multimerin family shapes the cancer landscape.The FEBS journal · 2026Review
- Rational design of hammerhead ribozymes as CD93 silencing tools for vascular diseases.Molecular therapy. Nucleic acids · 2026Article
- RAB5C Increases Endothelial Release of VWF by Regulating Vesicle Trafficking.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Heat shock protein 90 stabilizes CD93 glycosylation to influence angiogenesis during diabetic wound healing.Cellular & molecular biology letters · 2026Article
- CD93 in Health and Disease: Bridging Physiological Functions and Clinical Applications.International journal of molecular sciences · 2025Review
- Estimating progression of Alzheimer's disease with extracellular vesicle-related multi-omics risk models.Frontiers in aging neuroscience · 2025Article
- Global proteomics reveals pathways of mesenchymal stem cells altered by Mycobacterium tuberculosis.Scientific reports · 2024Article
- Structural insight into CD93 recognition by IGFBP7.Structure (London, England : 1993) · 2024Article
- Macrocephaly and developmental delay caused by missense variants in RAB5C.Human molecular genetics · 2023Article
- Identification of Potential Protein Targets in Extracellular Vesicles Isolated from Chemotherapy-Treated Ovarian Cancer Cells.Current issues in molecular biology · 2023Article
- Angiogenesis modulated by CD93 and its natural ligands IGFBP7 and MMRN2: a new target to facilitate solid tumor therapy by vasculature normalization.Cancer cell international · 2023Review
- Role of CD93 in Health and Disease.Cells · 2023Review
- A Bispecific METxMET Antibody-Drug Conjugate with Cleavable Linker Is Processed in Recycling and Late Endosomes.Molecular cancer therapeutics · 2023Article
- Chirality-biased protein expression profile during early stages of bone regeneration.Frontiers in bioengineering and biotechnology · 2023Article
- Reactive astrocytes transduce inflammation in a blood-brain barrier model through a TNF-STAT3 signaling axis and secretion of alpha 1-antichymotrypsin.Nature communications · 2022Article
- Rab GTPases as Modulators of Vascular Function.Cells · 2022Review
- Host Cell Signatures of the Envelopment Site within Beta-Herpes Virions.International journal of molecular sciences · 2022Review
- PUFA-DerivedACS chemical biology · 2022Article
- Immune checkpoint modulators in cancer immunotherapy: recent advances and emerging concepts.Journal of hematology & oncology · 2022Review
- Trafficking in blood vessel development.Angiogenesis · 2022Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the endothelium, the single-pass membrane protein CD93, through its interaction with the extracellular matrix protein Multimerin-2, activates signaling pathways that are critical for vascular development and angiogenesis. Trafficking of adhesion molecules through endosomal compartments modulates their signaling output. However, the mechanistic basis coordinating CD93 recycling and its implications for endothelial cell (EC) function remain elusive.
methodsHuman umbilical vein ECs (HUVECs) and human dermal blood ECs (HDBEC) were used in this study. Fluorescence confocal microscopy was employed to follow CD93 retrieval, recycling, and protein colocalization in spreading cells. To better define CD93 trafficking, drug treatments and transfected chimeric wild type and mutant CD93 proteins were used. The scratch assay was used to evaluate cell migration. Gene silencing strategies, flow citometry, and quantification of migratory capability were used to determine the role of Rab5c during CD93 recycling to the cell surface.
resultsHere, we identify the recycling pathway of CD93 following EC adhesion and migration. We show that the cytoplasmic domain of CD93, by its interaction with Moesin and F-actin, is instrumental for CD93 retrieval in adhering and migrating cells and that aberrant endosomal trafficking of CD93 prevents its localization at the leading edge of migration. Moreover, the small GTPase Rab5c turns out to be a key component of the molecular machinery that is able to drive CD93 recycling to the EC surface. Finally, in the Rab5c endosomal compartment CD93 forms a complex with Multimerin-2 and active β1 integrin, which is recycled back to the basolaterally-polarized cell surface by clathrin-independent endocytosis.
conclusionsOur findings, focusing on the pro-angiogenic receptor CD93, unveil the mechanisms of its polarized trafficking during EC adhesion and migration, opening novel therapeutic opportunities for angiogenic diseases.
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