Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 586, Issue -, Pages 27-33Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.11.030
Keywords
Angiogenesis; AMD; Rigidity; Endothelial cell; RPE; Contraction; Proliferation
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The study reveals the underlying role of the PI3K/Akt/mTOR signaling pathway in regulating vascular endothelial growth factor-A (VEGF-A) mediated signaling and functions. The pathway is activated on stiffer substrates, amplified by VEGF-A stimulation, and correlated with enhanced endothelial cell (EC) proliferation, contraction, pro-angiogenic secretion, and capillary-like tube formation. These findings have important implications for understanding age-related macular degeneration and provide insight into potential therapeutic pathways.
While it is now well-established that substrate stiffness regulates vascular endothelial growth factor-A (VEGF-A) mediated signaling and functions, causal mechanisms remain poorly understood. Here, we report an underlying role for the PI3K/Akt/mTOR signaling pathway. This pathway is activated on stiffer substrates, is amplified by VEGF-A stimulation, and correlates with enhanced endothelial cell (EC) proliferation, contraction, pro-angiogenic secretion, and capillary-like tube formation. In the settings of advanced age-related macular degeneration, characterized by EC and retinal pigment epithelial (RPE)mediated angiogenesis, these data implicate substrate stiffness as a novel causative mechanism and Akt/ mTOR inhibition as a novel therapeutic pathway. (C) 2021 Elsevier Inc. All rights reserved.
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