Related Experiment Video
Updated: Mar 27, 2026

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers
Published on: November 8, 2024
Tetraspanin CD151 and integrin α6β1 mediate platelet-enhanced endothelial colony forming cell angiogenesis
Z Huang1, X Miao1, M Patarroyo2
1Clinical Pharmacology Unit, Department of Medicine-Solna, Karolinska Institutet, Stockholm, Sweden.
Unlabelled:
ESSENTIALS: Platelet releasates (PRs) enhance endothelial colony forming cell (ECFC) angiogenesis. The impact of platelet membrane components on ECFC angiogenesis was studied by a tube formation assay. Platelets enhanced ECFC angiogenesis more potently than PR, via tetraspanin CD151 and integrin α6β1. Optimal enhancement of ECFC angiogenesis by platelets requires both membrane proteins and PR.
Background:
Platelets promote angiogenesis of endothelial colony forming cells (ECFCs), with the underlying mechanisms not being fully understood.
Objective:
To investigate if platelets regulate the angiogenic property of ECFCs via mechanisms beyond platelet-released angiogenic regulators.
Methods And Results:
Endothelial colony forming cells were generated by ECFC-directed cell culture of peripheral blood mononuclear cells. Capillary-like tube formation of ECFCs was assessed using a Matrigel assay. Platelets promoted ECFC tube formation in both basic and complete ECFC medium. Importantly, the ECFC angiogenic responses induced by platelets were stronger than those induced by platelet releasates. Thus, the branching points of ECFC tube formation (30.5 ± 9.0/field, ECFC alone) were increased by platelet releasates (58.2 ± 8.3/field) and even more profoundly by platelets (95.5 ± 17.6/field), indicating that platelet membrane components also promoted ECFC tube formation. The latter was further supported by evidence that fixed platelets did enhance ECFC tube formation. Subsequent experiments revealed that the promotion was dependent on platelet-surface glycoproteins, as removal of sialic acid from platelet glycoproteins by neuraminidase abolished the enhancement. Furthermore, platelet-expressed, but not ECFC-expressed, CD151 was important for the enhancement, as pretreatment of platelets, but not ECFCs, with a CD151-blocking antibody attenuated the effect. Integrin α6β1 on both ECFCs and platelets also participated in platelet-promoted tube formation, as integrin α6 or β1 blockade of either cell type markedly or totally inhibited the phenomenon. Moreover, platelets exerted the enhancement via the Src-PI3K signaling pathway of ECFCs.
Conclusion:
Platelet-enhanced ECFC angiogenesis requires platelet tetraspanin CD151 and α6β1 integrin, as well as ECFC α6β1 integrin and Src-PI3K signaling.
More Related Videos
08:50Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
Published on: April 9, 2018
11:18Real-time Imaging of Heterotypic Platelet-neutrophil Interactions on the Activated Endothelium During Vascular Inflammation and Thrombus Formation in Live Mice
Published on: April 2, 2013
Related Concept Videos
Intracellular Signaling Affects Focal Adhesions
Some...
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Activation of Integrins
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding...
Integrins
Some ECM proteins assemble into a basement membrane to which the remaining components adhere. Proteoglycans typically form the bulk of the ECM while fibrous proteins, like collagen,...
Selectins
Regulation of Angiogenesis and Blood Supply