miR‐30a‐5p inhibition promotes interaction of Fas+ endothelial cells and FasL+ microglia to decrease pathological neovascularization and promote physiological angiogenesis

Ischemia‐induced angiogenesis contributes to various neuronal and retinal diseases, and often results in neurodegeneration and visual impairment. Current treatments involve the use of anti‐VEGF agents but are not successful in all cases. In this study we determined that miR‐30a‐5p is another importa...

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Veröffentlicht in:	Glia 2019-02, Vol.67 (2), p.332-344
Hauptverfasser:	Murinello, Salome, Usui, Yoshihiko, Sakimoto, Susumu, Kitano, Maki, Aguilar, Edith, Friedlander, H. Maura, Schricker, Amelia, Wittgrove, Carli, Wakabayashi, Yoshihiro, Dorrell, Michael I., Westenskow, Peter D., Friedlander, Martin
Format:	Artikel
Sprache:	eng
Schlagworte:	Angiogenesis Animals Animals, Newborn Apoptosis Apoptosis - drug effects Apoptosis - genetics CCL2 Cell Line, Transformed Cell Proliferation - drug effects Cell Proliferation - genetics Cell survival Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Crosstalk Diabetes mellitus Diabetic retinopathy Disease Models, Animal Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism fas Receptor - metabolism FasL protein Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Humans Inhibition Ischemia Lectins - metabolism Mice Mice, Inbred C57BL Mice, Transgenic Microglia Microglia - metabolism MicroRNAs - genetics MicroRNAs - metabolism miR‐30a‐5p Monocyte chemoattractant protein 1 Neovascularization, Pathologic - drug therapy Neovascularization, Pathologic - metabolism Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Neurodegeneration Pathogenesis People with disabilities Phagocytes Repair Retina Retinopathy RNA Interference - physiology RNA, Messenger - metabolism Therapeutic applications Tissues Vascular endothelial growth factor Vascularization
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