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The microenvironmental abundance of VEGF and other proangiogenic factors drives continual angiogenesis and the production of an abnormal blood vessel network. Structurally, vessels are often dilated, weave a tortuous path, and show heterogeneity of distribution such that certain areas within a tumor are hypovascular and others hypervascular. At the cellular level, proangiogenic factors induce weakening of VE-Cadherin-mediated endothelial cell (EC) junctions and EC migration, altering vessel wall architecture. Similarly, the perivascular cells (PVCs, comprised of pericytes and vascular smooth muscle cells [VSMCs]) are often only loosely attached to ECs and are reduced in number. A number of important molecules regulate pericyte– EC interaction, including platelet-derived growth factor-B (PDGF-B), Ang-1, transforming growth factor-b(TGF-b), and sphingosine-1-phosphate (S1P) in healthy tissues. In tumors, proangiogenic factors promote PVCEC dissociation, however. For example, VEGF induces the formation ofVEGFR-PDGFRbcomplexes in pericytes, which impede PDGFRbmediated adherence of ECs to pericytes. Finally, the perivascular basement membrane (BM) is also structurally abnormal in tumors—excessively thin or absent in certain regions and abnormally thick in others. |
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