[Erratum] Oxidative stress, autophagy and pyroptosis in the neovascularization of oxygen­induced retinopathy in mice.

Subsequently to the publication of this paper, the authors have realized that Figs. 2 and 5 have been published containing the same GAPDH control protein bands. After having examined the final proofs of this article, the control blots were indeed different comparing between the figures, and regrettably an error concerning Fig. 2 was made during the final stages of the proof preparation. The corrected version of Fig. 2, including the correct GAPDH protein bands, is shown opposite. Note that the error that occurred with this Figure during production process did not affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The Editor of Molecular Medicine Reports apologizes to the authors and to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 19: 927-934, 2019; DOI: 10.3892/mmr.2018.9759].

Oxidative stress, autophagy and pyroptosis in the neovascularization of oxygen­induced retinopathy in mice.

Retinal neovascularization (RNV) is a principal cause of visual impairment and blindness worldwide. The present study aimed to investigate how oxidative stress, autophagy and pyroptosis alter in RNV. The oxygen­induced retinopathy (OIR) model was established in C57BL/6J mice by exposing them to a high concentration of oxygen. RNV was clearly visible in the fundus images and was qualitatively analyzed by counting the number of neovascular endothelial cell nuclei at postnatal day 17. Subsequently, the expression of vascular endothelial growth factor (VEGF)­A and hypoxia­inducible factor­1α (HIF­1α) at the protein level were measured. Furthermore, oxidative stress was examined using dihydroethidium (DHE) staining, and NADPH oxidase (NOX) 1 and 4 in the retinas were detected using reverse transcription­quantitative polymerase chain reaction analysis. Additionally, immunostaining of microtubule associated protein 1 light chain 3α (LC3) was performed and the expression levels of the LC3, p62, autophagy protein (Atg)5, Atg7, Atg12, Beclin1, NOD­like receptor family pyrin domain­containing 3 (NLRP3), caspase­1, interleukin (IL)­1ß, pro­caspase­1 and pro­IL­1ß proteins were determined using western blotting in order to detect pyroptosis and autophagic flux. Autophagosomes were also detected using transmission electron microscopy. The results revealed that VEGF­A and HIF­1α protein expression levels, the DHE­positive area, and NOX1 and NOX4 mRNA expression levels were significantly increased in the OIR mice. Furthermore, increased levels of NLRP3, caspase­1, IL­1ß, pro­caspase­1 and pro­IL­1ß proteins demonstrated that pyroptosis was activated. However, an accumulation of p62 and a reduction in the levels of LC3II/I and autophagosomes indicated that autophagic flux was compromised. Therefore, elevated levels of reactive oxygen species and pyroptosis along with attenuated autophagy were demonstrated in the OIR mice. The combination of oxidative stress, pyroptosis and impaired autophagy may serve an important role in the pathophysiology of RNV and may be a potential target to prevent RNV.