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Small extracellular vesicles derived from human induced pluripotent stem cell-differentiated neural progenitor cells mitigate retinal ganglion cell degeneration in a mouse model of optic nerve injury

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Neural Regeneration Research 2025年第2期20卷 587-597页

作者： Tong Li Hui-Min Xing Hai-Dong Qian Qiao Gao Sheng-Lan Xu Hua Ma Zai-Long Chi State Key Laboratory of Ophthalmology Optometry and Visual ScienceEye HospitalWenzhou Medical UniversityWenzhouZhejiang ProvinceChina National Clinical Research Center for Ocular Diseases Eye HospitalWenzhou Medical UniversityWenzhouZhejiang ProvinceChina

Several studies have found that transplantation of neural progenitor cells(NPCs)promotes the survival of injured neurons.However,a poor integration rate and high risk of tumorigenicity after cell transplantation limits their clinical application.Small extracellular vesicles(sEVs)contain bioactive molecules for neuronal protection and regeneration.Previous studies have shown that stem/progenitor cell-derived sEVs can promote neuronal survival and recovery of neurological function in neurodegenerative eye diseases and other eye diseases.In this study,we intravitreally transplanted sEVs derived from human induced pluripotent stem cells(hiPSCs)and hiPSCs-differentiated NPCs(hiPSC-NPC)in a mouse model of optic nerve crush.Our results show that these intravitreally injected sEVs were ingested by retinal cells,especially those localized in the ganglion cell layer.Treatment with hiPSC-NPC-derived sEVs mitigated optic nerve crush-induced retinal ganglion cell degeneration,and regulated the retinal microenvironment by inhibiting excessive activation of microglia.Component analysis further revealed that hiPSC-NPC derived sEVs transported neuroprotective and anti-inflammatory miRNA cargos to target cells,which had protective effects on RGCs after optic nerve injury.These findings suggest that sEVs derived from hiPSC-NPC are a promising cell-free therapeutic strategy for optic neuropathy.

关键词： exosome miRNA neural progenitor cell neurodegeneration neuroinflammation neuroprotection optic nerve crush optic neuropathy retinal ganglion cell small extracellular vesicles

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cell replacement with stem cell-derived retinal ganglion cells from different protocols

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Neural Regeneration Research 2024年第4期19卷 807-810页

作者： Ziming Luo Kun-Che Chang Spencer Center for Vision Research Byers Eye InstituteStanford University School of Medicine Department of Ophthalmology Louis J.Fox Center for Vision RestorationUniversity of Pittsburgh School of Medicine Department of Neurobiology Center of NeuroscienceUniversity of Pittsburgh School of Medicine

Glaucoma,characterized by a degenerative loss of retinal ganglion cells,is the second leading cause of blindness worldwide.There is currently no cure for vision loss in glaucoma because retinal ganglion cells do not regenerate and are not replaced after injury.Human stem cell-derived retinal ganglion cell transplant is a potential therapeutic strategy for retinal ganglion cell degenerative diseases.In this review,we first discuss a 2D protocol for retinal ganglion cell differentiation from human stem cell culture,including a rapid protocol that can generate retinal ganglion cells in less than two weeks and focus on their transplantation outcomes.Next,we discuss using 3D retinal organoids for retinal ganglion cell transplantation,comparing cell suspensions and clusters.This review provides insight into current knowledge on human stem cell-derived retinal ganglion cell differentiation and transplantation,with an impact on the field of regenerative medicine and especially retinal ganglion cell degenerative diseases such as glaucoma and other optic neuropathies.

关键词： cell clumps cell suspension cell transplantation differentiation direct-induced protocol glaucoma optic neuropathy regenerative medicine retinal ganglion cell retinal organoids stem cells

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OTX2 stimulates adult retinal ganglion cell regeneration

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Neural Regeneration Research 2022年第3期17卷 690-696页

作者： Raoul Torero Ibad Nicole Quenech’du Alain Prochiantz Kenneth L.Moya Centre for Interdisciplinary Research in Biology(CIRB) Collége de FranceCNRS UMR 7241INSERM U1050Labex MemoLifeParis Sciences et Lettres Research UniversityParisFrance

retinal ganglion cell(RGC) axons provide the only link between the light sensitive and photon transducing neural retina and visual centers of the brain.RGC axon degeneration occurs in a number of blinding diseases and the ability to stimulate axon regeneration from surviving ganglion cells could provide the anatomic substrate for restoration of vision.OTX2 is a homeoprotein transcription factor expressed in the retina and previous studies showed that,in response to stress,exogenous OTX2 increases the in vitro and in vivo survival of RGCs.Here we examined and quantified the effects of OTX2 on adult RGC axon regeneration in vitro and in vivo.The results show that exogenous OTX2 stimulates the regrowth of axons from RGCs in cultures of dissociated adult retinal cells and from explants of adult retinal tissue and that RGCs respond directly to OTX2 as regrowth is observed in cultures of purified adult rat RGCs.Importantly,after nerve crush in vivo,we observed a positive effect of OTX2 on the number of regenerating axons up to the optic chiasm within 14 days post crush and a very modest level of acuity absent in control mice.The effect of OTX2 on RGC survival and regeneration is of potential interest for degenerative diseases affecting this cell type.All animal procedures were approved by the local "Comié d'éιthique en expérimentation animale n°59" and authorization n° 00702.01 delivered March 28,2014 by the French "Ministére de l'enseignement supérieur et de la recherche".

关键词： axon regeneration dissociated retinal culture GAP-43 homeoprotein optic nerve crush OTX2 retinal explants retinal ganglion cell

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The role of miRNA in retinal ganglion cell health and disease

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Neural Regeneration Research 2022年第3期17卷 516-522页

作者： Ben Mead Stanislav Tomarev School of Optometry and Vision Sciences Cardiff UniversityCardiffUK Section of retinal ganglion cell Biology Laboratory of Retinal Cell and Molecular BiologyNational Eye InstituteNational Institutes of HealthBethesdaMDUSA

miRNA are short non-coding RNA responsible for the knockdown of proteins through their targeting and silencing of complimentary m RNA sequences.The mi RNA landscape of a cell thus affects the levels of its proteins and has significant consequences to its health.Deviations in this mi RNA landscape have been implicated in a variety of neurodegenerative diseases and have also garnered interest as targets for treatment.retinal ganglion cells are the sole projection neuron of the retina with their axons making up the optic nerve.They are a focus of study not only for their importance in vision and the myriad of blinding diseases characterized by their dysfunction and loss,but also as a model of other central nervous system diseases such as spinal cord injury and traumatic brain injury.This review summarizes current knowledge on the role of mi RNA in retinal ganglion cell function,highlighting how perturbations can result in disease,and how modulating their abundance may provide a novel avenue of therapeutic research.

关键词： exosome extracellular vesicle glaucoma miRNA neurodegenerative disease optic neuropathy retina retinal ganglion cell

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Regulatory mechanisms of retinal ganglion cell death in normal tension glaucoma and potential therapies

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Neural Regeneration Research 2023年第1期18卷 87-93页

作者： Wen-Cui Shen Bing-Qing Huang Jin Yang Tianjin Eye Hospital&Eye Institute Tianjin Key Laboratory of Ophthalmology and Visual ScienceNankai UniversityTianjinChina State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood DiseasesInstitute of Hematology&Blood Diseases HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeTianjinChina

Normal tension glaucoma(NTG)is a multifactorial optic neuropathy characterized by normal intraocular pressure,progressive retinal ganglion cell(RGC)death,and glaucomatous visual field loss.Recent studies have described the mechanisms underlying the pathogenesis of NTG.In addition to controlling intraocular pressure,neuroprotection and reduction of RGC degeneration may be beneficial therapies for NTG.In this review,we summarized the main regulatory mechanisms of RGC death in NTG,including autophagy,glutamate neurotoxicity,oxidative stress,neuroinflammation,immunity,and vasoconstriction.Autophagy can be induced by retinal hypoxia and axonal damage.In this process,ischemia can cause mutations of optineurin and activate the nuclear factor-kappa B pathway.Glutamate neurotoxicity is induced by the over-stimulation of N-methyl-D-aspartate membrane receptors by glutamate,which occurs in RGCs and induces progressive glaucomatous optic neuropathy.Oxidative stress also participates in NTG-related glaucomatous optic neuropathy.It impairs the mitochondrial and DNA function of RGCs through the apoptosis signal-regulating kinase-JUN N-terminal kinase pathway.Moreover,it increases inflammation and the immune response of RGCs.Endothelin 1 causes endothelial dysfunction and impairment of ocular blood flow,promoting vasospasm and glaucomatous optic neuropathy,as a result of NTG.In conclusion,we discussed research progress on potential options for the protection of RGCs,including TANK binding kinase 1 inhibitors regulating autophagy,N-methyl-D-aspartate receptor antagonists inhibiting glutamate toxicity,ASK1 inhibitors regulating mitochondrial function,and antioxidants inhibiting oxidative stress.In NTG,RGC death is regulated by a network of mechanisms,while various potential targets protect RGCs.Collectively,these findings provide insight into the pathogenesis of NTG and potential therapeutic strategies.

关键词： autophagy endothelin 1 glutamate neurotoxicity inhibitor nerve regeneration neuroinflammation normal tension glaucoma oxidative stress retinal ganglion cell vasoconstriction

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Cholesterol homeostasis regulated by ABCA1 is critical for retinal ganglion cell survival

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Science China(Life Sciences) 2023年第2期66卷 211-225页

作者： Jialiang Yang Yuhong Chen Tongdan Zou Bai Xue Fang Yang Xiangzhou Wang Yibo Huo Boyun Yan Yuxia Xu Shiyu He Yi Yin Jing Wang Xiong Zhu Lin Zhang Yu Zhou Zhengfu Tai Ping Shuai Man Yu Qian Luo Yilian Cheng Bo Gong Xianjun Zhu Jing Zhang Xinghuai Sun Ying Lin Houbin Zhang Zhenglin Yang Key Laboratory for Human Disease Gene Study of Sichuan Province and Institute of Laboratory Medicine Sichuan Provincial People’s HospitalUniversity of Electronic Science and Technology of ChinaChengdu 610072China Department of Ophthalmology and Visual Science Eye and Ear Nose Throat(ENT)HospitalFudan UniversityShanghai 200032China School of Optoelectronic Science and Engineering University of Electronic Science and Technology of ChinaChengdu 611731China Institute of Chengdu Biology Sichuan Translational Medicine HospitalChinese Academy of SciencesChengdu 610093China Department of Ophthalmology Sichuan Provincial People’s HospitalUniversity of Electronic Science and Technology of ChinaChengdu 610072China Research Unit for Blindness Prevention of Chinese Academy of Medical Sciences Sichuan Academy of Medical Sciences&Sichuan Provincial People’s HospitalChengdu 610072China

Genome-wide association studies have suggested a link between primary open-angle glaucoma and the function of ABCA1.ABCA1 is a key regulator of cholesterol efflux and the biogenesis of high-density lipoprotein(HDL) particles. Here, we showed that the POAG risk allele near ABCA1 attenuated ABCA1 expression in cultured cells. Consistently, POAG patients exhibited lower ABCA1 expression, reduced HDL, and higher cholesterol in white blood cells. Ablation of Abca1 in mice failed to form HDL, leading to elevated cholesterol levels in the retina. Counting retinal ganglion cells(RGCs) by using an artificial intelligence(AI) program revealed that Abca1-deficient mice progressively lost RGCs with age. Single-cell RNA sequencing(scRNA-seq) revealed aberrant oxidative phosphorylation in the Abca1-/-retina, as well as activation of the mTORC1 signaling pathway and suppression of autophagy. Treatment of Abca1-/-mice using atorvastatin reduced the cholesterol level in the retina,thereby improving metabolism and protecting RGCs from death. Collectively, we show that lower ABCA1 expression and lower HDL are risk factors for POAG. Accumulated cholesterol in the Abca1-/-retina causes profound aberrant metabolism, leading to a POAG-like phenotype that can be prevented by atorvastatin. Our findings establish statin use as a preventive treatment for POAG associated with lower ABCA1 expression.

关键词： ABCA1 glaucoma retinal ganglion cell HDL cholesterol atorvastatin

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Resveratrol prevents hypoxia-induced retinal ganglion cell death related with ErbB2

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International Journal of Ophthalmology(English edition) 2022年第3期15卷 394-400页

作者： Hyemin Seong Joo Yeon Jeong Jinhyun Ryu Juyeong Park Yong‑Seop Han Hyun-Kyung Cho Seong Jae Kim Jong Moon Park Sang Soo Kang Seong Wook Seo Department of Ophthalmology Institute of Health SciencesCollege of MedicineGyeongsang National UniversityJinjuGyeongnam 52727Republic of Korea Department of Anatomy and Convergence Medical Science Institute of Health SciencesCollege of MedicineGyeongsang National UniversityJinjuGyeongnam 52727Republic of Korea Department of Ophthalmology Gyeongsang National University Changwon HospitalGyeongsang National UniversityCollege of MedicineChangwon 51472Republic of Korea

AIM: To confirm the changes in proteins related with hypoxia-induced retinal cell death and to assess the effects of resveratrol(Res).METHODS: The therapeutic effect of Res was verified using an ischemic/reperfusion(I/R) model in vivo and a hypoxia modelin retinal ganglion cells(RGCs) in vitro.Death of RGCs were confirmed by TUNEL assay.Protein expression was confirmed by Western blotting and immunohistochemistry.In addition, flow cytometric analysis was used to confirm the response in the cell unit to obtain more accurate data.RESULTS: ErbB2 expression and apoptosis in the ganglion cell layer(GCL) increased after I/R injury.Treatment of Res rescued I/R-induced ganglion cell death, downregulated apoptosis and ErbB2 protein expression in the retina.In subsequent in vitro models, Res affects apoptosis by regulating the phosphorylation and expression of mouse double minute 2 homolog(MDM2), along with those of ErbB2.These results suggest that Res reverses GCL-specific apoptosis via downregulation of ErbB2 in ischemic injury.CONCLUSION: In light of Res favorable properties, it should be evaluated in the treatment of RGC death and related retinal disease characterized by ErbB2 and MDM2 expression.Therefore, Res is appropriate therapeutic agent for treating ischemic injury-related eye diseases by targeting the expression of ErbB2 and MDM2.

关键词： ischemia/reperfusion injury hypoxia retinal ganglion cell resveratrol ErbB2

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retinal ganglion cell death in a DBA/2J mouse model of glaucoma Microglial activation and intraocular pressure

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Neural Regeneration Research 2010年第4期5卷 273-281页

作者： Liping Yang Xiujuan Guo Lingling Wu Ying Li Lemeng Wu Dongmei Wang Mark O.M.TsoO Peking University Third Hospital Peking University Eye Center Beijing 100191 China Wilmer Eye Institute JohnsHopkins University School of Medicine Baltimore MD 21287 USA

BACKGROUND： retinal microglia has been shown to reactivate in a murine model of pigmentary glaucoma. However, the relationship between microglial activation and intraocular pressure （lOP） elevation and retinal ganglion cell （RGC） death is still unclear. OBJECTIVE： To verify that microglial activation and tumor necrosis factor alpha （TNF-α） expression is involved in RGC death with elevated lOP and prolonged time of glaucomatous optic nerve lesion in a DBA/2J mouse model of glaucoma. DESIGN, TIME AND SETTING： This randomized, controlled, animal experiment was performed at the Peking University Third Hospital, Peking University Eye Center, China between December 2006 and May 2008.MATEFIiALS： DBA/2J mice and C57BL/6J mice （Jackson Laboratory, USA）, rat anti-mouse CD11 b monoclonal antibody （Serotec, UK）, and goat anti-TNF-α polyclonal antibody （Sigma, USA） were used in this study.METHODS： A total of 100 female, DBA/2J mice at 3, 6, 9, 12, and 14 months of age （20 mice per age group） were used for the glaucoma model, and 18 C57BL/6J mice at 3, 9, 14 months of age （6 mice per age group） were used as normal controls. The anterior segment of the eye was observed using a slit-lamp biomicroscope, lOP was measured using a microneedle system. Morphology and number of retinal microglia were observed using immunohistochemistry. RGCs were quantified using Nissl staining. Co-localization of TNF-α and microglia was observed using double-labeling immunofluorescence. Excavation of the optic nerve head was observed utilizing hematoxylin-eosin staining. MAIN OUTCOME MEASURES： The following parameters were measured： lOP levels, numbers of RGCs and activated microglia, and TNF-α expression. RESULTS： In 6-month-old DBA/2J mice, dispersed pigment was observed, and some mice developed increased IOP. At 9 months of age, lOP levels reached a peak. In 3-month-old DBA/2J mice, microglia were activated. In 6-month-old DBA/2J mice, the number of activated microglia was significantly increased and migrated to the outer retinal layer. In 9-month-

关键词： pigmentary glaucoma DBA/2J mice microglia retinal ganglion cell tumor necrosis factor-α

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Inhibition of retinal ganglion cell apoptosis: regulation of mitochondrial function by PACAP

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Neural Regeneration Research 2018年第5期13卷 923-929页

作者： Huan-Huan Cheng Hui Ye Rui-Ping Peng Juan Deng Yong Ding Department of Ophthalmology the Third Affiliated Hospital of Sun Yat-sen University Department of Ophthalmology The First Affiliated Hospital of Jinan University

Pituitary adenylate cyclase-activating polypeptide（PACAP） is an endogenous peptide with neuroprotective effects on retinal neurons, but the precise mechanism underlying these effects remains unknown. Considering the abundance of mitochondria in retinal ganglion cells（RGCs）, we postulate that the protective effect of PACAP is associated with the regulation of mitochondrial function. RGC-5 cells were subjected to serum deprivation for 48 hours to induce apoptosis in the presence or absence of 100 nM PACAP. As revealed with the cell Counting Kit-8 assay, PACAP at different concentrations significantly increased the viability of RGC-5 cells. PACAP also inhibited the excessive generation of reactive oxygen species in RGC-5 cells subjected to serum deprivation. We also showed by flow cytometry that PACAP inhibited serum deprivation-induced apoptosis in RGC-5 cells. The proportions of apoptotic cells and cells with mitochondria depolarization were significantly decreased with PACAP treatment. Western blot assays demonstrated that PACAP increased the levels of Bcl-2 and inhibited the compensatory increase of PAC1. Together, these data indicate protective effects of PACAP against serum deprivation-induced apoptosis in RGCs, and that the mechanism of this action is associated with maintaining mitochondrial function.

关键词： nerve regeneration pituitary adenylate cyclase-activating polypeptide pituitary adenylate cyclase-activating polypeptide receptor type 1 serum deprivation apoptosis retinal ganglion cell retinal ganglion cell-5 glaucoma mitochondria neural regeneration

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β-Ⅲ-Tubulin: a reliable marker for retinal ganglion cell labeling in experimental models of glaucoma

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International Journal of Ophthalmology(English edition) 2015年第4期8卷 643-652页

作者： Shan-Ming Jiang Li-Ping Zeng Ji-Hong Zeng Li Tang Xiao-Ming Chen Xin Wei Department of Ophthalmology West China Hospital Sichuan University

·AIM: To evaluate the reliability of β-III-Tubulin protein as a retinal ganglion cell(RGC) marker in the experimental glaucoma model.·METHODS: Glaucoma mouse models were established by injecting polystyrene microbeads into the anterior chamber of C57BL/6J mice, then their retinas were obtained 14 d and 28 d after the intraocular pressure(IOP)was elevated. retinal flat mounts and sections were double-labeled by fluorogold(FG) and β-III-Tubulin antibody or single-labeled by β-III-Tubulin antibody,then RGCs were counted and compared respectively.· RESULTS: IOP of the injected eyes were elevated significantly and reached the peak at 22.8 ±0.7 mm Hg by day 14 after injection, then dropped to 11.3 ±0.7 mm Hg by day 28. RGC numbers counted by FG labeling and β-III- Tubulin antibody labeling were 64 807 ± 4930 and64 614 ±5054 respectively in the control group, with no significant difference. By day 14, RGCs in the experimental group decreased significantly compared to the control group, but there was no significant difference between the FG labeling counting and the β-III-Tubulin antibody labeling counting either in the experimental group or in the control group. The result was similar by day 28, with further RGC loss.·CONCLUSION: Our result suggested that the β-III-Tubulin protein was not affected by IOP elevation and can be used as a reliable marker for RGC in experimental models of glaucoma.

关键词： β-III-Tubulin glaucoma fluorogold retinal ganglion cell

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