The granulation tissue formation phase of wound repair relies heavily on neovascularization, expanding the limits of O2 and nutrient diffusion into tissues through the development of new blood vessels. Vasculogenesis is the mechanism of formation of new vessels by vascular progenitor cells that instinctively self-assemble. However, the main focus of this article is angiogenesis, the growth of pre-existing blood vessels to produce new vessels. Angiogenesis is controlled by soluble factors released from the wound site such as vascular endothelial growth factor (VEGF) which activates human microvascular endothelial cells (HMVE) to begin sprouting and extending, forming the lumen within the mature capillaries and undergoing functional anastomosis. However, microenvironmental signals also come into play in the multistep process through mechanical forces transmitted by the extracellular matrix (ECM) as physical interactions between cells and ECM change cell shape and cytoskeletal structure. Furthermore, altering the elasticity, adhesiveness, or topography of the ECM, applying mechanical stress, or changing the tensile force generated by the cells can also make changes to the shape and function of the hair cells. Although regional variations in ECM mechanics and cell shape appear to mediate the formation of three-dimensional tissue patterns resulting from the growth and differentiation of neighboring cells, the underlying mechanism that controls gene transcription for angiogenic control through ECM-borne mechanical signals that It assembles with growth factors still remains unknown. Many diseases result from deregulation of angiogenesis, which is counteracted by US Food and Drug Administration-approved angiogenesis inhibitors that target the key soluble factor, VEGF, but pay no attention to how they mecha... half of paper. .. ...motor activity and expression mediated by mechanosensitive signaling pathways to regulate capillary blood vessel formation. This could lead to new therapeutic advances with specific modifiers to combat angiogenesis-dependent diseases. Because both neurons and endothelial cells in the retina express VEGFR2, in vivo findings may not specifically address endothelial cells. Neuron-vessel interactions also play an important role in vascular development and therefore further analysis of transcriptional modification of both aspects could help to understand the importance of VEGFR2. Similar to previous protocols, the different expressions of transcription factors on neurons will map a clearer control mechanism. Convergent expression of VEGFR2 with the endothelium thus demonstrates the balance between microvasculature signaling function and capillary morphogenesis.