Abstract
The 37kDa/67kDa laminin receptor (LRP/LR) is a central receptor mediating interactions between tumour cells and the basement membrane and is thereby a key player in adhesion and invasion, essential processes in metastatic cancer. To affect continued tumour growth, tumours induce angiogenesis for the constant delivery of nutrients and oxygen. This study aims to determine the blocking effect of the anti-LRP/LR specific antibody, W3 on the angiogenic potential of HUVE (human umbilical vein endothelial) cells. Flow cytometric analysis revealed that 97% of HUVE cells display cell surface LRP/LR. An angiogenesis assay was conducted employing HUVE cells seeded on the basement membrane reconstituent Matrigel™ supplemented with the pro-angiogenic factor vascular endothelial growth factor (VEGF). Post 18h incubation at 37°C tubular structures, namely tube lengths were assessed. Treatment of established tubular structures with 100 µg/ml anti-LRP/LR specific antibody completely blocked angiogenesis. Our findings suggest a central role of the 37kDa/67kDa LRP/LR in tube formation and recommends anti-LRP/LR specific antibodies as potential therapeutic tools for treatment of tumour angiogenesis.
Highlights
Angiogenesis, the formation of new blood vessels from preexisting capillaries[1], is a physiologically vital process involved in embryonic development, wound healing; the female menstrual cycle, tissue growth[1] and vascular remodeling.[2]
As LRP/LR is a key receptor in mediating cellular adhesion, proliferation and migration, mediating the cellular effects of laminin-1 and has previously been implicated in angiogenesis, we examined whether the receptor was expressed on the surface of the human umbilical vein endothelial (HUVE) cell model employed in this study
The rate-limiting step in the angiogenic process is the degradation of the basement membrane which is promptly followed by endothelial cell detachment, proliferation and reorganisation into tubular structures
Summary
Angiogenesis, the formation of new blood vessels from preexisting capillaries[1], is a physiologically vital process involved in embryonic development, wound healing; the female menstrual cycle, tissue growth[1] and vascular remodeling.[2] This process is highly regulated in healthy individuals. The vascular endothelial growth factor (VEGF), is the principle angiogenic inducer.[6,7,8] Angiogenesis is a multistep process involving endothelial cell activation and subsequent degradation of the surrounding extracellular matrix or basal lamina.[1] This results in protease activation and subsequent release of pro-angiogenic factors/ peptides which in turn stimulate endothelial cell migration towards the angiogenic signal, proliferation and differentiation.[1,3]
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