Autophagy-induced regression of hyaloid vessels in early ocular development

Yang, Esther; Lee, Byung J.; Kim, Jin Hee; Kim, Kyu W.; Yu, Young Suk; Kim, Jeong H.

doi:10.4161/auto.6.7.13306

Cited by 32 publications

(24 citation statements)

References 19 publications

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“…Autophagy as a response to hypoxia has also been recently implicated in the regression of hyaloid vessels in early developing retina. 36 Here, we conclude that Beclin 1 is associated with the suppression of angiogenesis. However, it remains unclear whether active autophagy is required for the anti-angiogenic effects of Beclin 1, or whether the results reflect a regulatory signaling function of Beclin 1 that is independent of autophagy.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 59%

Beclin 1 deficiency is associated with increased hypoxia-induced angiogenesis

et al. 2011

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Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 59%

Beclin 1 deficiency is associated with increased hypoxia-induced angiogenesis

et al. 2011

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“…5c). In addition, while autophagy has been implicated in angiogenesis 41,42 , we saw no consistent or reproducible abnormalities in Atg7 endo mice when post-natal retinal angiogenesis was assessed (Fig. 5d).…”

Section: Resultsmentioning

confidence: 78%

Autophagy regulates endothelial cell processing, maturation and secretion of von Willebrand factor

Torisu

Lee

et al. 2013

Nat Med

220

200

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Endothelial secretion of von Willebrand factor (VWF) from intracellular organelles known as Weibel-Palade bodies (WPBs) is required for platelet adhesion to the injured vessel wall. Here, we demonstrate that WPBs are in some cases found near or within autophagosomes and that endothelial autophagosomes contain abundant VWF protein. Pharmacological inhibitors of autophagy, or knockdown of the essential autophagy genes Atg5 or Atg7, inhibits the in vitro secretion of VWF. Furthermore, while mice with an endothelial specific deletion of Atg7 have normal vessel architecture and capillary density, these animals exhibit impaired epinephrine-stimulated VWF release, reduced levels of high molecular weight VWF multimers and a corresponding elevation of their bleeding times. Endothelial deletion of Atg5 or pharmacological inhibition of autophagic flux results in a similar in vivo alteration of hemostasis. Thus, autophagy regulates endothelial VWF secretion and transient pharmacological inhibition of autophagic flux may be a useful strategy to prevent thrombotic events.

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“…Targeting MTOR signaling is quite pertinent in neuroblastoma as it negatively regulates autophagy, a cellular process involved in the degradation of long-lived proteins. 16 Recent studies have identified a novel role for autophagy in inhibiting angiogenesis, 11,12 and therefore, we set out to explore whether autophagy might regulate the degradation of GRP, a critical proangiogenic factor in human neuroblastomas.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 This process has recently been identified as a physiological response to hypoxia-induced-angiogenesis and regression of hyaloid vessels. 11,12 Autophagy may potentially regulate angiogenesis by the lysosome-dependent degradation of hypoxia-inducible factor HIF1A/HIF-1α, a proangiogenic factor. 13 GRP undergoes degradation by a lysosomal or a phosphoramidon-sensitive pathway.…”

Section: Introductionmentioning

confidence: 99%