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- W2247454121 abstract "Abstract The communication between vascular endothelial cells (ECs) and pericytes in the microvasculature is fundamental for vascular growth and homeostasis; however, these processes are disrupted by diabetes. Here we show that modulation of p75 NTR expression in ECs exposed to high glucose activates transcription of miR-503, which negatively affects pericyte function. p75 NTR activates NF-κB to bind the miR-503 promoter and upregulate miR-503 expression in ECs. NF-κB further induces activation of Rho kinase and shedding of endothelial microparticles carrying miR-503, which transfer miR-503 from ECs to vascular pericytes. The integrin-mediated uptake of miR-503 in the recipient pericytes reduces expression of EFNB2 and VEGFA , resulting in impaired migration and proliferation. We confirm operation of the above mechanisms in mouse models of diabetes, in which EC-derived miR-503 reduces pericyte coverage of capillaries, increased permeability and impaired post-ischaemic angiogenesis in limb muscles. Collectively, our data demonstrate that miR-503 regulates pericyte–endothelial crosstalk in microvascular diabetic complications." @default.
- W2247454121 created "2016-06-24" @default.
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- W2247454121 date "2015-08-13" @default.
- W2247454121 modified "2023-10-01" @default.
- W2247454121 title "p75NTR-dependent activation of NF-κB regulates microRNA-503 transcription and pericyte–endothelial crosstalk in diabetes after limb ischaemia" @default.
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- W2247454121 doi "https://doi.org/10.1038/ncomms9024" @default.
- W2247454121 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4538859" @default.
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