Lipidomics dataset of PTEN deletion-induced optic nerve regeneration mouse model

Arcuri, Jennifer; Hegarty, Shane V.; He, Zhigang; Bhattacharya, Sanjoy K.

doi:10.1016/j.dib.2020.106699

Cited by 6 publications

(3 citation statements)

References 5 publications

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“…DR-induced PTEN overexpression promotes retinal neuronal cells death [35]. RGCs lossmediated optic nerve injury is closely associated with the increase in PTEN [36]. Importantly, PTEN is widely proven as an antagonist of the AKT signaling pathway, which can upregulate NRF2 expression to alleviate oxidative damage and ROS release [37].…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4

Sun

Zhu

et al. 2022

Stem Cell Res Ther

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Background As a leading cause of vision decline and severe blindness in adults, diabetic retinopathy (DR) is characterized by the aggravation of retinal oxidative stress and apoptosis in the early stage. Emerging studies reveal that mesenchymal stem cells-derived small extracellular vesicles (MSC-sEV) treatment represents a promising cell-free approach to alleviate ocular disorders. However, the repairing effects of MSC-sEV in DR remain largely unclear. This study aimed at exploring the role and the underlying mechanism of MSC-sEV in hyperglycemia-induced retinal degeneration. Methods In vivo, we used streptozotocin (STZ) to establish diabetic rat model, followed by the intravitreal injection of MSC-sEV to determine the curative effect. The cell viability and antioxidant capacity of retinal pigment epithelium (RPE) cells stimulated with high-glucose (HG) medium after MSC-sEV treatment were analyzed in vitro. By detecting the response of cell signaling pathways in MSC-sEV-treated RPE cells, we explored the functional mechanism of MSC-sEV. Mass spectrometry was performed to reveal the bioactive protein which mediated the role of MSC-sEV. Results The intravitreal injection of MSC-sEV elicited antioxidant effects and counteracted retinal apoptosis in STZ-induced DR rat model. MSC-sEV treatment also reduced the oxidative level and enhanced the proliferation ability of RPE cells cultured in HG conditions in vitro. Further studies showed that the increased level of phosphatase and tensin homolog (PTEN) inhibited AKT phosphorylation and nuclear factor erythroid 2-related factor 2 (NRF2) expression in RPE cells stimulated with HG medium, which could be reversed by MSC-sEV intervention. Through mass spectrometry, we illustrated that MSC-sEV-delivered neuronal precursor cell-expressed developmentally downregulated 4 (NEDD4) could cause PTEN ubiquitination and degradation, activate AKT signaling and upregulate NRF2 level to prevent DR progress. Moreover, NEDD4 knockdown impaired MSC-sEV-mediated retinal therapeutic effects. Conclusions Our findings indicated that MSC-sEV ameliorated DR through NEDD4-induced regulation on PTEN/AKT/NRF2 signaling pathway, thus revealing the efficiency and mechanism of MSC-sEV-based retinal protection and providing new insights into the treatment of DR.

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Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4

Sun

Zhu

et al. 2022

Stem Cell Res Ther

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“…Even in this area a number of innovative approaches are emerging. Our large‐scale multi‐omics analyses (Arcuri et al, 2020; Arcuri et al, 2021; Chauhan et al, 2020; Trzeciecka, Carmy, et al, 2019) combined with computer language processing and machine‐learning (Khosla et al, 2021; Myer et al, 2020) has helped identify convergent pathways for axon regeneration and the critical lipids and metabolites in them. The critical knowledge gap is how the first steps of recognition of a target neuron occur by the growing axon and what are the steps in the sequence that results in growth cone collapse leading to formation of an actual functional synapse formation (Skaper et al, 2001; Spencer et al, 1998).…”

Section: The Current Treatment Modalities and Real Gap Towards Interv...mentioning

confidence: 99%

Appropriate patient population for future visual system axon regeneration therapies

Bhattacharya,

Alabiad,

Kishor

2023

WIREs Mechanisms of Disease

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A number of blinding diseases caused by damage to the optic nerve result in progressive vision loss or loss of visual acuity. Secondary glaucoma results from traumatic injuries, pseudoexfoliation or pigmentary dispersion syndrome. Progressive peripheral vision loss is common to all secondary glaucoma irrespective of the initial event. Axon regeneration is a potential therapeutic avenue to restore lost vision in these patients. In contrast to the usual approach of having the worst possible patient population for initial therapies, axon regeneration may require consideration of appropriate patient population even for initial treatment trials. The current state of axon regeneration therapies, their potential future and suitable patient population when ready is discussed in this perspective. The selection of patients are important for adoption of axon regeneration specifically in the areas of central nervous system regenerative medicine.This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology Neurological Diseases > Biomedical Engineering Metabolic Diseases > Molecular and Cellular Physiology

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“…The optic nerve crush (ONC) is a commonly used model to study optic nerve injury and glaucoma in addition to the survival and regeneration of retinal ganglion cells (RGCs) [1,2] and the effects of drug or other therapeutic interventions on RGCs [3][4][5][6][7][8]. It provides good repeatability and simple operation.…”

Section: Introductionmentioning

confidence: 99%

Optic nerve injury models under varying forces

et al. 2022

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Purpose To explore the pathological changes in optic nerve injury models under varying forces. Methods The rats were classified into 4 groups: sham operation (SH), 0.1, 0.3, and 0.5 N. Modeling was performed using the lateral optic nerve pulling method. Seven days after modeling, Brn3a immunofluorescence was used to detect retinal ganglion cell (RGC) number, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to detect RGC apoptosis, and flash visual evoked potential (FVEP) was used to detect the optic nerve function on days 1, 3, and 7 after modeling. In addition, LC3 II and P62 expression levels in retinal tissues were detected by western blotting to observe the changes in autophagy levels. Results RGC number decreased 7 d after modeling, and it showed a downward trend with increasing damaging force. The number of apoptotic RGCs in ganglion cell layer in the 0.3 and 0.5 N groups was increased and was higher than that in the 0.1 N group. The difference in FVEP of rats in each group was mainly reflected in the P2 peak latency. LC3 II and P62 expression levels in retinal tissue of 0.3 and 0.5 N groups were higher than those of the SH and 0.1 groups; however, the difference between the 0.1 N and SH groups was not statistically significant. Conclusion Precisely controlling the force of the optic nerve clamping injury model is necessary because different forces acting on the optic nerve will lead to differences in the loss of optic neurons, the conduction function of the optic nerve, and autophagy level in retinal tissues.

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Lipidomics dataset of PTEN deletion-induced optic nerve regeneration mouse model

Cited by 6 publications

References 5 publications

Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4

Mesenchymal stem cells-derived small extracellular vesicles alleviate diabetic retinopathy by delivering NEDD4

Appropriate patient population for future visual system axon regeneration therapies

Optic nerve injury models under varying forces

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