MiR-93-5p targeting PTEN regulates the NMDA-induced autophagy of retinal ganglion cells via AKT/mTOR pathway in glaucoma

Li, Rui; Jin, Yiping; Li, Qian; Sun, Xinghuai; Zhu, Haohao; Cui, Hongping

doi:10.1016/j.biopha.2018.01.044

Cited by 63 publications

(44 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, an investigation reported that miR-93 was downregulated in N-methyl-D-aspartate-treated glaucoma rats and RGCs in vitro. The upregulation of miR-93, which targets phosphatase and tensin homologue, suppressed the autophagy of RGCs through the AKT/mTOR pathway 37 .…”

Section: Fig 5 Overexpression Of Mir-93 Inhibited Microglial Migratimentioning

confidence: 99%

MicroRNA-93/STAT3 signalling pathway mediates retinal microglial activation and protects retinal ganglion cells in an acute ocular hypertension model

et al. 2021

View full text Add to dashboard Cite

Glaucoma is a common neurodegenerative disease and a leading cause of irreversible blindness worldwide. Retinal microglia-mediated neuroinflammation is involved in the process of optic nerve damage, but the mechanisms driving this microglial activation remain mostly elusive. Previous investigations reported that microRNAs are associated with the retinal microglial reaction and neural apoptosis. In the present study, we found that microRNA-93-5p (miR-93) played a key role in the reaction of retinal microglial cells in vivo and in vitro. The miR-93 level was significantly reduced in the retinae of rat acute ocular hypertension (AOH) models, which were accompanied by retinal microglial activation, overproduction of inflammatory cytokines, and subsequent retinal ganglion cells (RGCs) death, versus the retinae of controls. The induction of miR-93 overexpression significantly reduced microglial proliferation, migration and cytokine release, inhibited the expression of the target gene signal transducer and activator of transcription 3 (STAT3) and p-STAT3, and was associated with a reduced loss of RGCs. Treatment with a STAT3 inhibitor also decreased retinal microglial activation after AOH injury. Taken together, these results suggest that the miR-93/STAT3 pathway is directly related to the downregulation of retinal microglia-mediated neuro-inflammation and showed a neuroprotective effect. Regulating microglial activation through miR-93 may serve as a target for neuroprotective therapy in pathological ocular hypertension.

show abstract

Section: Fig 5 Overexpression Of Mir-93 Inhibited Microglial Migratimentioning

confidence: 99%

MicroRNA-93/STAT3 signalling pathway mediates retinal microglial activation and protects retinal ganglion cells in an acute ocular hypertension model

et al. 2021

View full text Add to dashboard Cite

show abstract

“…PTEN can inhibit the activation of AKT, causing suppression of the PI3K/AKT/mTOR signaling [ 76 , 80 , 81 ]. MiRNAs, such as miR-93-5p and miR-21, can regulate autophagy via the pathways involving PTEN [ 82 , 83 ]. In our study, both in vivo and in vitro experiments showed that PoPTEN knockdown attenuated ATG5 and beclin 1 expression and promoted AKT and mTOR expression, whereas PoPTEN overexpression produced the opposite effects.…”

Section: Discussionmentioning

confidence: 99%

Phosphatase and Tensin Homolog (PTEN) of Japanese Flounder—Its Regulation by miRNA and Role in Autophagy, Apoptosis and Pathogen Infection

Guan

Sun

2020

IJMS

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are small non-coding RNAs with important roles in diverse biological processes including immunity. Japanese flounder (Paralichthys olivaceus) is an aquaculture fish species susceptible to the infection of bacterial and viral pathogens including Edwardsiella tarda. In a previous study, pol-miR-novel_547, a novel miRNA of flounder with unknown function, was found to be induced by E. tarda. In the present study, we investigated the regulation and function of pol-miR-novel_547 and its target gene. We found that pol-miR-novel_547 was regulated differently by E. tarda and the viral pathogen megalocytivirus, and pol-miR-novel_547 repressed the expression of PTEN (phosphatase and tensin homolog) of flounder (PoPTEN). PoPTEN is ubiquitously expressed in multiple tissues of flounder and responded to bacterial and viral infections. Interference with PoPTEN expression in flounder cells directly or via pol-miR-novel_547 promoted E. tarda invasion. Consistently, in vivo knockdown of PoPTEN enhanced E. tarda dissemination in flounder tissues, whereas in vivo overexpression of PoPTEN attenuated E. tarda dissemination but facilitated megalocytivirus replication. Further in vitro and in vivo studies showed that PoPTEN affected autophagy activation via the AKT/mTOR pathway and also modulated the process of apoptosis. Together these results reveal for the first time a critical role of fish PTEN and its regulatory miRNA in pathogen infection, autophagy, and apoptosis.

show abstract

“…Recently, a study suggested that miR-93-5p suppressed the differentiation and migration of neurons [15]. In addition, another study suggested that miR-93-5p decreased the VEGF and IL-8-dependent angiogenesis in neuroblastoma cells [25]. miR-93-5p has also been shown to affect autophagy in retinal ganglionic cells via AKT/mTOR pathway [26].…”

Section: Discussionmentioning

confidence: 99%

miR-93-5p attenuates apoptosis and autophagy by regulating SRY-box2 in spinal cord-injured rats in vivo and PC12 cells in vitro

et al. 2020

Arch Med Sci

View full text Add to dashboard Cite

Introduction: In the current work we studied the involvement of miR-93-5p in spinal cord injury (SCI) by involving SCI rats and LPS-mediated injuries in PC12 cells. Material and methods: The PC12 cells were exposed to LPS in order to induce cell injury that mimicked the in vitro model of spinal cord injury. The in vivo model was created by submitting rats to contusion injury. The cell apoptosis and viability were evaluated by flow cytometry and cell counting kit (CCK-8). The expression of various apoptosis and autophagy-related proteins was done by western blot assay. Results: The treatment of LPS caused cell injuries in PC12 cells. The levels of miR-93-5p were suppressed in LPS-injured cells. Over-expression of miR-93-5p decreased autophagy and apoptosis and increased cell viability in LPS injured cells via up-regulation of SRY-box2. Up-regulation of SRY-box2 ameliorated LPS-mediated cell injury whereas suppression of SRY-box2 accelerated the LPS-mediated cell injury. Also, upregulation of miR-93-5p blocked the JAK/STAT and MAPK/ERK pathways via up-regulating the expression of SRY-box2. Treatment in SCI rats with miR-93-5p agomir inhibited cell apoptosis and autophagy. Conclusions: The results of the study confirmed the attenuating role of miR-93-5p against cell autophagy and apoptosis in LPS-injured PC12 cells and SCI rats via up-regulation of the expression of SRY-box2.

show abstract

MiR-93-5p targeting PTEN regulates the NMDA-induced autophagy of retinal ganglion cells via AKT/mTOR pathway in glaucoma

Cited by 63 publications

References 23 publications

MicroRNA-93/STAT3 signalling pathway mediates retinal microglial activation and protects retinal ganglion cells in an acute ocular hypertension model

MicroRNA-93/STAT3 signalling pathway mediates retinal microglial activation and protects retinal ganglion cells in an acute ocular hypertension model

Phosphatase and Tensin Homolog (PTEN) of Japanese Flounder—Its Regulation by miRNA and Role in Autophagy, Apoptosis and Pathogen Infection

miR-93-5p attenuates apoptosis and autophagy by regulating SRY-box2 in spinal cord-injured rats in vivo and PC12 cells in vitro

Contact Info

Product

Resources

About