Tetraspanin CD151 and integrin α6β1 mediate platelet-enhanced endothelial colony forming cell angiogenesis.

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Abstract

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.

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Most cited references 30

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Angiogenesis in life, disease and medicine.

Peter Carmeliet (2005)

The growth of blood vessels (a process known as angiogenesis) is essential for organ growth and repair. An imbalance in this process contributes to numerous malignant, inflammatory, ischaemic, infectious and immune disorders. Recently, the first anti-angiogenic agents have been approved for the treatment of cancer and blindness. Angiogenesis research will probably change the face of medicine in the next decades, with more than 500 million people worldwide predicted to benefit from pro- or anti-angiogenesis treatments.

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Integrin-regulated FAK-Src signaling in normal and cancer cells.

Satyajit K. Mitra, David Schlaepfer (2006)

Integrins can alter cellular behavior through the recruitment and activation of signaling proteins such as non-receptor tyrosine kinases including focal adhesion kinase (FAK) and c-Src that form a dual kinase complex. The FAK-Src complex binds to and can phosphorylate various adaptor proteins such as p130Cas and paxillin. In normal cells, multiple integrin-regulated linkages exist to activate FAK or Src. Activated FAK-Src functions to promote cell motility, cell cycle progression and cell survival. Recent studies have found that the FAK-Src complex is activated in many tumor cells and generates signals leading to tumor growth and metastasis. As both FAK and Src catalytic activities are important in promoting VEGF-associated tumor angiogenesis and protease-associated tumor metastasis, support is growing that FAK and Src may be therapeutically relevant targets in the inhibition of tumor progression.

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Redefining endothelial progenitor cells via clonal analysis and hematopoietic stem/progenitor cell principals.

Mervin C. Yoder, Laura Mead, Daniel Prater … (2006)

The limited vessel-forming capacity of infused endothelial progenitor cells (EPCs) into patients with cardiovascular dysfunction may be related to a misunderstanding of the biologic potential of the cells. EPCs are generally identified by cell surface antigen expression or counting in a commercially available kit that identifies "endothelial cell colony-forming units" (CFU-ECs). However, the origin, proliferative potential, and differentiation capacity of CFU-ECs is controversial. In contrast, other EPCs with blood vessel-forming ability, termed endothelial colony-forming cells (ECFCs), have been isolated from human peripheral blood. We compared the function of CFU-ECs and ECFCs and determined that CFU-ECs are derived from the hematopoietic system using progenitor assays, and analysis of donor cells from polycythemia vera patients harboring a Janus kinase 2 V617F mutation in hematopoietic stem cell clones. Further, CFU-ECs possess myeloid progenitor cell activity, differentiate into phagocytic macrophages, and fail to form perfused vessels in vivo. In contrast, ECFCs are clonally distinct from CFU-ECs, display robust proliferative potential, and form perfused vessels in vivo. Thus, these studies establish that CFU-ECs are not EPCs and the role of these cells in angiogenesis must be re-examined prior to further clinical trials, whereas ECFCs may serve as a potential therapy for vascular regeneration.

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Author and article information

Journal

Journal ID (iso-abbrev): J. Thromb. Haemost.

Title: Journal of thrombosis and haemostasis : JTH

Publisher: Wiley

ISSN (Electronic): 1538-7836

ISSN (Print): 1538-7836

Publication date (Electronic): Mar 2016

Volume: 14

Issue: 3

Affiliations

[1 ] Clinical Pharmacology Unit, Department of Medicine-Solna, Karolinska Institutet, Stockholm, Sweden.

[2 ] Department of Dental Medicine, Department of Medicine-Solna, Karolinska Institutet, Stockholm, Sweden.

[3 ] Clinical Immunology and Allergy Unit, Department of Medicine-Solna, Karolinska Institutet, Stockholm, Sweden.

[4 ] Cardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital-Solna, Stockholm, Sweden.

Article

DOI: 10.1111/jth.13248

PubMed ID: 26749288

SO-VID: 1f96eaec-44e4-40db-8769-8b24058dad3c

History

Keywords: platelets,integrin α6β1,angiogenesis,CD151 protein,endothelial cells

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Keywords: platelets, integrin α6β1, angiogenesis, CD151 protein, endothelial cells

Tetraspanin CD151 and integrin α6β1 mediate platelet-enhanced endothelial colony forming cell angiogenesis.

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Abstract

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Gamma Delta T cells

Most cited references 30

Angiogenesis in life, disease and medicine.

Integrin-regulated FAK-Src signaling in normal and cancer cells.

Redefining endothelial progenitor cells via clonal analysis and hematopoietic stem/progenitor cell principals.

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Journal

Affiliations

Article

History

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