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Regulation of retinal angiogenesis by endothelial nitric oxide synthase signaling pathway

View Article: PubMed Central - PubMed

ABSTRACT

Angiogenesis plays an essential role in embryo development, tissue repair, inflammatory diseases, and tumor growth. In the present study, we showed that endothelial nitric oxide synthase (eNOS) regulates retinal angiogenesis. Mice that lack eNOS showed growth retardation, and retinal vessel development was significantly delayed. In addition, the number of tip cells and filopodia length were significantly reduced in mice lacking eNOS. Retinal endothelial cell proliferation was significantly blocked in mice lacking eNOS, and EMG-2-induced endothelial cell sprouting was significantly reduced in aortic vessels isolated from eNOS-deficient mice. Finally, pericyte recruitment to endothelial cells and vascular smooth muscle cell coverage to blood vessels were attenuated in mice lacking eNOS. Taken together, we suggest that the endothelial cell function and blood vessel maturation are regulated by eNOS during retinal angiogenesis.

No MeSH data available.


Related in: MedlinePlus

eNOS regulates pericyte recruitment and VSMC coverage(A and B) Retinas from the wild type and eNOS knockout mice at P6 were stained with IB4 (blue) and either pericyte marker protein (NG2, red, panel A) or VSMC marker protein (SM22α, red, panel B). Images were visualized under a confocal microscope at ×40 magnification. Scale bars, 100 µm.
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Figure 4: eNOS regulates pericyte recruitment and VSMC coverage(A and B) Retinas from the wild type and eNOS knockout mice at P6 were stained with IB4 (blue) and either pericyte marker protein (NG2, red, panel A) or VSMC marker protein (SM22α, red, panel B). Images were visualized under a confocal microscope at ×40 magnification. Scale bars, 100 µm.

Mentions: We next explored the role of eNOS in the stabilization and maturation of blood vessels. As shown in Fig. 4A, retinas isolated from mice lacking eNOS showed a significant reduction in pericyte recruitment of endothelial cells, especially in the periphery rather than the ON site. In addition, VSMC coverage to blood vessels was significantly impaired in mice lacking eNOS (Fig. 4B). These results indicate that eNOS regulates blood vessel stabilization through pericyte recruitment and VSMC coverage.


Regulation of retinal angiogenesis by endothelial nitric oxide synthase signaling pathway
eNOS regulates pericyte recruitment and VSMC coverage(A and B) Retinas from the wild type and eNOS knockout mice at P6 were stained with IB4 (blue) and either pericyte marker protein (NG2, red, panel A) or VSMC marker protein (SM22α, red, panel B). Images were visualized under a confocal microscope at ×40 magnification. Scale bars, 100 µm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5015000&req=5

Figure 4: eNOS regulates pericyte recruitment and VSMC coverage(A and B) Retinas from the wild type and eNOS knockout mice at P6 were stained with IB4 (blue) and either pericyte marker protein (NG2, red, panel A) or VSMC marker protein (SM22α, red, panel B). Images were visualized under a confocal microscope at ×40 magnification. Scale bars, 100 µm.
Mentions: We next explored the role of eNOS in the stabilization and maturation of blood vessels. As shown in Fig. 4A, retinas isolated from mice lacking eNOS showed a significant reduction in pericyte recruitment of endothelial cells, especially in the periphery rather than the ON site. In addition, VSMC coverage to blood vessels was significantly impaired in mice lacking eNOS (Fig. 4B). These results indicate that eNOS regulates blood vessel stabilization through pericyte recruitment and VSMC coverage.

View Article: PubMed Central - PubMed

ABSTRACT

Angiogenesis plays an essential role in embryo development, tissue repair, inflammatory diseases, and tumor growth. In the present study, we showed that endothelial nitric oxide synthase (eNOS) regulates retinal angiogenesis. Mice that lack eNOS showed growth retardation, and retinal vessel development was significantly delayed. In addition, the number of tip cells and filopodia length were significantly reduced in mice lacking eNOS. Retinal endothelial cell proliferation was significantly blocked in mice lacking eNOS, and EMG-2-induced endothelial cell sprouting was significantly reduced in aortic vessels isolated from eNOS-deficient mice. Finally, pericyte recruitment to endothelial cells and vascular smooth muscle cell coverage to blood vessels were attenuated in mice lacking eNOS. Taken together, we suggest that the endothelial cell function and blood vessel maturation are regulated by eNOS during retinal angiogenesis.

No MeSH data available.


Related in: MedlinePlus