Abstract
Bone marrow contains endothelial progenitor cells (EPCs) that, upon pro-angiogenic stimuli, migrate and differentiate into endothelial cells (ECs) and contribute to re-endothelialization and neo-vascularization. There are currently no reliable markers to characterize EPCs, leading to their inaccurate identification. In the past, we showed that, in a panel of tumors, some cells on the vessel wall co-expressed CD14 (monocytic marker) and CD31 (EC marker), indicating a putative differentiation route of monocytes into ECs. Herein, we disclosed monocytes as potential EPCs, using in vitro and in vivo models, and also addressed the cancer context. Monocytes acquired the capacity to express ECs markers and were able to be incorporated into blood vessels, contributing to cancer progression, by being incorporated in tumor neo-vasculature. Reactive oxygen species (ROS) push monocytes to EC differentiation, and this phenotype is reverted by cysteine (a scavenger and precursor of glutathione), which indicates that angiogenesis is controlled by the interplay between the oxidative stress and the scavenging capacity of the tumor microenvironment.
Highlights
Tumor angiogenesis is essential to provide oxygen and nutrients to cancer cells, and to remove waste products from the tumor microenvironment
In the line with the morphological changes observed in cultured monocytes, a dynamic CD31 gain and CD14 loss was observed during 17 days in culture, in the presence of vascular endothelial growth factor (VEGF)
Blood vessels are signed with “V”. In addition to their relevance in sprouting angiogenesis, endothelial progenitor cells (EPCs) circulation, mobilization, and differentiation play an essential role in the repair of injured vessels [4,5,6]
Summary
Tumor angiogenesis is essential to provide oxygen and nutrients to cancer cells, and to remove waste products from the tumor microenvironment. Over the last two decades, cancer treatment using anti-angiogenic therapies has fallen short of expectations [3], showing that the mechanisms underlying neovascularization in cancer are not fully understood. This failure can be explained, at least in part, by the fact that the specific origin of endothelial progenitor cells (EPCs) is not yet determined. Different studies reported EPCs as essential in restoring injured vessels. EPCs belong to a subset of cells, arising from hematopoietic stem cells in bone marrow; upon pro-angiogenic stimuli, they proliferate, migrate, and differentiate into endothelial cells (ECs) [4,5,6]
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