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Incorporating Pericytes into an Endothelial Cell Bead Sprouting Assay

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Published on: February 16, 2018

Endothelial-stromal interactions in angiogenesis.

Christopher C W Hughes¹

¹Department of Molecular Biology & Biochemistry, University of California Irvine, Irvine, California 92697, USA. cchughes@uci.edu

Current Opinion in Hematology

|April 9, 2008

Summary

This review explores how tumor stroma components like fibroblasts and pericytes interact with endothelial cells. Understanding these interactions is key to developing new anti-angiogenesis therapies for cancer.

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Area of Science:

Cell Biology
Oncology
Biomedical Engineering

Background:

Angiogenesis, the formation of new blood vessels, is crucial for wound healing and tumor growth.
Tumor stroma comprises various cells and extracellular matrix components that influence angiogenesis.
Endothelial cells are central to angiogenesis, interacting with stromal cells and matrix.

Purpose of the Study:

To review recent findings on the interactions between angiogenic endothelial cells and stromal components.
To highlight the roles of fibroblasts and pericytes in tumor angiogenesis.
To discuss the extracellular matrix's contribution to new blood vessel formation.

Main Methods:

Review of recent scientific literature.
Analysis of gene expression data.
Focus on molecular mechanisms of angiogenesis.

Main Results:

Fibroblasts play a critical role in tumor growth and angiogenesis, influencing tumor cell phenotype.
Gene expression arrays reveal fibroblast diversity and their impact on the tumor microenvironment.
Pericytes are increasingly recognized for their role in regulating angiogenesis and as potential therapeutic targets.
Advances elucidate the 'soil and seed' hypothesis at a molecular level.

Conclusions:

Angiogenesis initiation involves basement membrane degradation, endothelial cell sprouting, and pericyte regulation.
Fibroblasts and myofibroblasts synchronize angiogenic events via extracellular matrix molecules and growth factors.
Fibroblast growth factors and transforming growth factor beta are key regulators in this process.