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A modified chronic ocular hypertension rat model for retinal ganglion cell neuroprotection

Frontiers of Medicine 2013年第3期7卷 367-377页

作者： Lichun Zhong ocular Science Department Toxikon CorporationBedfordMA 01730USA

This study aimed to modify a chronic ocular hypertension(OHT)rat model to screen for potential compounds to protect retinal ganglion cells(RGCs)from responding to increased intraocular pressure(IOP).A total of 266 rats were prepared and randomly grouped according to different time-points,namely,weeks 3,8,16,and *** were sedated and eye examination was performed to score as the corneal damage on a scale of 1 to *** OHT rat model was created via the injection of a hypertonic saline solution into the episcleral veins once weekly for two *** was identified when the IOP at week 0 was≥6 mmHg than that at week-2 for the same *** RGCs were labeled by injecting 4%*** were sacrificed,and the eyes were enucleated and *** fixed retinas were dissected to prepare flat *** viable RGCs were visualized and *** IOP(meanβ±βSD)was calculated,and data were analyzed by the paired t-test and one-way *** OHT model was created in 234 of 266 rats(87.97%),whereas 32 rats(12.03%)were removed from the study because of the absence of IOP elevation(11.28%)and/or corneal damage scores over 4(0.75%).IOP was elevated by as much as 81.35%for 24 *** average IOP was(16.68β±β0.98)βmmHg in non-OHT eyes(n=234),but was(27.95±0.97)βmmHg in OHT eyes(n=234).Viable RGCs in the OHT eyes were significantly decreased in a time-dependent manner by 29.41%,38.24%,55.32%,and 59.30%at weeks 3,8,16,and 24,respectively,as compared to viable RGCs in the non-OHT eyes(P<β0.05).The OHT model was successfully created in 88%of the *** IOP in the OHT eyes was elevated by approximately 81%for 24 *** number of viable RGCs was decreased by 59%of the rats in a time-dependent *** modified OHT model may provide an effective and reliable method for screening drugs to protect RGCs from glaucoma.

关键词： chronic ocular hypertension intraocular pressure retinal ganglion cells neuroprotection glaucoma

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Neuroprotective effect of mesenchymal stem cellderived extracellular vesicles on optic nerve injury in chronic ocular hypertension

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Neural Regeneration Research 2023年第10期18卷 2301-2306页

作者： Fei Yu Yao Wang Chang-Quan Huang Si-Jie Lin Ru-Xin Gao Ren-Yi Wu Department of Glaucoma Eye Institute and Affiliated Xiamen Eye Center of Xiamen UniversitySchool of MedicineXiamen UniversityXiamenFujian ProvinceChina Fujian Provincial Key Laboratory of Corneal&ocular Surface Diseases XiamenFujian ProvinceChina Shaanxi Provincial Key Lab of Ophthalmology Shaanxi Clinical Study Center for Ocular DiseaseShaanxi Institute of OphthalmologyFirst Affiliated HospitalMedical SchoolNorthwest UniversityXi’anShaanxi ProvinceChina Eye Institute of Xiamen University Fujian Provincial Key Laboratory of Ophthalmology and Visual ScienceXiamenFujian ProvinceChina Department of Glaucoma Shanghai Peace Eye HospitalShanghaiChina

Mesenchymal stem cells have neuroprotective effects that limit damage to the retina and photoreceptors,and which may be mediated by extracellular vesicles(or exosomes)released by mesenchymal stem *** investigate the neuroprotective effect of extracellular vesicles derived from umbilical cord mesenchymal stem cells on glaucoma,we established rat models of chronic ocular hypertension by injecting conjunctival fibroblasts into the anterior chamber to mimic optic nerve injury caused by *** week after injury,extracellular vesicles derived from umbilical cord-derived mesenchymal stem cells were injected into the vitreous *** found that extracellular vesicles derived from mesenchymal stem cells substantially reduced retinal damage,increased the number of retinal ganglion cells,and inhibited the activation of *** findings suggest that mesenchymal stem cell-derived extracellular vesicles can help alleviate optic nerve injury caused by chronic ocular hypertension,and this effect is achieved by inhibiting cell apoptosis.

关键词： animal model apoptosis chronic glaucoma chronic ocular hypertension extracellular vesicles mesenchymal stem cells neuroprotection rat retinal ganglion cells umbilical cord

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TGF-β_1 in retinal ganglion cells in rats with chronic ocular hypertension: its expression and anti-apoptotic effect

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International Journal of Ophthalmology(English edition) 2011年第4期4卷 396-401页

作者： Yong-Jian Tao 1, Dian-Wen Gao 1, Miao Yu 2 1Department of Ophthalmology, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China 2 Shenyang Pharmaceutical University, Shenyang 110016, Liaoning Province, China Department of Ophthalmology Shengjing Hospital of China Medical University Shenyang 110004 Liaoning Province China.

AIM: To investigate the anti-apoptotic effect of transforming growth factor beta-1 (TGF-β1) on chronic ocular hypertension. METHODS: The expression of TGF-β1 in retinal ganglion cells (RCGs) was measured using the immunohistochemiscal S-P method and real-time PCR in the normally control group, the ocular hypertension group (experimental group A), the ocular hypertension plus antibody intervention group (experimental group B) and the ocular hypertension plus antigen intervention group (experimental group C) at 1, 2, 3 and 4 weeks postoperatively. The count of apoptotic RCGs was measured using the TUNEL method. RESULTS: The expression of TGF-β1 was significantly higher in experimental group C than that in other three groups (Pchronic ocular hypertension.

关键词： glaucoma nerve protect TGF-β1 retinal ganglion cells chronic ocular hypertension

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Phosphorylation of NR2A at Ser1232 by CDK5/P35 contributes to retinal ganglion cell death in rat chronic ocular hypertension model

Phosphorylation of NR2A at Ser1232 by CDK5/P35 contributes t...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Jie CHEN,Yan-Ying MIAO,Xiao-Han WANG,Xiong-Li YANG,Zhong-Feng WANG~* Institute of Neurobiology,Institutes of Brain Science and State Key Laboratory of Medical Neurobiology,Fudan University,Shanghai 200032,China

＜正＞For glaucoma,a major cause of blindness,elevated intraocular pressure is an important risk *** loss and dysfunction in glaucoma result from selective death of retinal ganglion cells（RGCs）.In the present study,we explored if and how cyclin-dependent kinase 5（CDK5） and its activator P35,which have been shown to contribute to pathogenesis of neurodegenerative diseases,may be involved in RGC death in rat chronic ocular hypertension（COH） *** rat COH model was produced by ligating and cauterizing the episcleral veins of right *** retinas were collected at 1,2,3, 4 and 6 weeks after *** survival and apoptosis of RGC were examined by CTB-retrograde labeling technique and TUNEL assay,*** expression of CDK5/P35 and phospho-NR2A at Serl232（pNR2A-S1232）,aphosphorylation site of CDK5,were detected by Western blot and immunohistochemistry,and the relationship of CDK5/P35 and pNR2A-S1232 was assayed by *** results showed that the number of RGCs was significantly decreased from 4 weeks after operation,and RGCs were labeled TUNEL positive at week 4 after operation in the COH *** the other hand,the immunoreactivity of P35 and pNR2A-S 1232 was found at the RGC *** to sham group,the expression of pNR2A-S1232 in COH group was significantly decreased after 2 weeks,which was followed by a prominent increase from week 3 to week 6,with a peak at week *** change in expression of P35 with time showed a similar *** changes in pNR2A-S1232 and P35 were in parallel to those in survival and apoptosis of ***, a direct interaction between CDK5 and pNR2A-S1232 was shown by ***,the present work demonstrated that CDK5/P35-mediated phosphorylation of NR2A at Ser1232 may contribute to the RGC death in rat COH model.

关键词： CDK5/P35 pNR2A-S1232 retina apoptosis chronic ocular hypertension

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mGluR I-mediated inhibition of Kir channels contributes to retinal Mller cell gliosis in a rat chronic ocular hypertension model

mGluR I-mediated inhibition of Kir channels contributes to r...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Min JI~(1,2,4),Yan-Ying MIAO~(1,3,4),Ling-Dan DONG~(1,3,4),Jie CHEN~(1,3,4),Xiao-Fen MO~(1,2,4),Xing-Huai SUN~(1,2,4),Zhong-Feng WANG~(1,3,4,*) 1 Institutes of Brain Science and 2 Eye & ENT Hospital,3 Institute of Neurobiology and 4 State Key Laboratory of Medical Neurobiology,Fudan University,Shanghai,China

Mller cell gliosis is a universal response in many retinal pathological conditions,including glaucoma. Accompanying the enhanced expression of glial fibrillary acidic protein(GFAP),the Kir K channel is downregulated in most,if not all,retinal *** mechanisms underlying Mller cell gliosis and the downregulation of K currents are poorly ***,we show that Mller cell Kir currents were reduced significantly and GFAP expression was increased in a rat chronic ocular hypertension(COH)*** group I mGluR agonist DHPG mimicked the COH-induced suppression of Kir currents,and this was selectively blocked by the mGluR5 antagonist *** intracellular Ca-dependent PLC/IP-ryanodine/PKC signaling pathway mediated the DHPG ***-induced changes in Mller cells were eliminated by injecting MPEP and were mimicked by an intravitreal injection of ***,mGluR5-mediated suppression of Kir currents contributed to retinal Mller cell gliosis in a rat COH model.

关键词： mGluR I retinal Mller cell gliosis Kir K+ channel chronic ocular hypertension

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L-and T-type Ca^(2+)channels dichotomously contribute to retinal ganglion cell injury in experimental glaucoma

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Neural Regeneration Research 2023年第7期18卷 1570-1577页

作者： Hong-Ning Wang Wen-Jing Qian Guo-Li Zhao Fang Li Yan-Ying Miao Bo Lei Xing-Huai Sun Zhong-Feng Wang State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science Institutes of Brain ScienceFudan UniversityShanghaiChina Institutes of Neuroscience and Third Affiliated Hospital Henan Provincial People’s HospitalHenan Eye InstituteHenan Eye HospitalPeople’s Hospital of Zhengzhou UniversityZhengzhou UniversityZhengzhouHenan ProvinceChina Eye Institute and Department of Ophthalmology Eye&ENT HospitalNHC Key Laboratory of MyopiaShanghai Key Laboratory of Visual Impairment and RestorationFudan UniversityShanghaiChina

Retinal ganglion cell apoptotic death is the main pathological characteristic of glaucoma,which is the leading cause of irreversible *** of Ca^(2+)homeostasis plays an important role in ***-gated Ca^(2+)channel blockers have been shown to improve vision in patients with ***,whether and how voltage-gated Ca^(2+)channels are involved in retinal ganglion cell apoptotic death are largely *** this study,we found that total Ca^(2+)current densities in retinal ganglion cells were reduced in a rat model of chronic ocular hypertension experimental glaucoma,as determined by whole-cell patch-clamp electrophysiological *** analysis showed that L-type Ca^(2+)currents were downregulated while T-type Ca^(2+)currents were upregulated at the later stage of *** blot assay and immunofluorescence experiments confirmed that expression of the Ca_(V)1.2 subunit of L-type Ca^(2+)channels was reduced and expression of the Ca_(V)3.3 subunit of T-type Ca^(2+)channels was increased in retinas of the chronic ocular hypertension *** tumor necrosis factor-α,an important inflammatory factor,inhibited the L-type Ca^(2+)current of isolated retinal ganglion cells from control rats and enhanced the T-type Ca^(2+)*** changes were blocked by the tumor necrosis factor-αinhibitor XPro1595,indicating that both types of Ca^(2+)currents may be mediated by soluble tumor necrosis factor-α.The intracellular mitogen-activated protein kinase/extracellular signal-regulated kinase pathway and nuclear factor kappa-B signaling pathway mediate the effects of tumor necrosis factor-α.TUNEL assays revealed that mibefradil,a T-type calcium channel blocker,reduced the number of apoptotic retinal ganglion cells in the rat model of chronic ocular *** results suggest that T-type Ca^(2+)channels are involved in disrupted Ca^(2+)homeostasis and apoptosis of retinal ganglion cells in glaucoma,and application of T-type

关键词： apoptosis CaV1.2 CaV3.3 chronic ocular hypertension extracellular signal-regulated kinase mitogen-activated protein kinase nuclear factor-kappa B patch-clamp retina tumor necrosis factor-α

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P2X7/P2X4 Receptors Mediate Proliferation and Migration of Retinal Microglia in Experimental Glaucoma in Mice

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Neuroscience Bulletin 2022年第8期38卷 901-915页

作者： Meng-Xi Xu Guo-Li Zhao Xin Hu Han Zhou Shu-Ying Li Fang Li Yanying Miao Bo Lei Zhongfeng Wang State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science Institutes of Brain ScienceFudan UniversityShanghai200032China Institute of Neuroscience and Third Affiliated Hospital Henan Provincial People’s HospitalHenan Eye InstituteHenan Eye HospitalPeople’s Hospital of Zhengzhou UniversityZhengzhou UniversityZhengzhou450003China

Microglia are involved in the inflammatory response and retinal ganglion cell damage in ***,we investigated how microglia proliferate and migrate in a mouse model of chronic ocular hypertension(COH).In COH retinas,the microglial proliferation that occurred was inhibited by the P2X7 receptor(P2X7R)blocker BBG or P2X7R knockout,but not by the P2X4R blocker *** of primary cultured microglia with BzATP,a P2X7R agonist,mimicked the effects of cell proliferation and migration in COH retinas through the intracellular MEK/ERK signaling *** migration assays showed that the P2X4R agonist CTP induced microglial migration,which was completely blocked by *** vivo and in vitro experiments demonstrated that ATP,released from activated Müller cells through connexin43 hemichannels,acted on P2X7R to induce microglial proliferation,and acted on P2X4R/P2X7R(mainly P2X4R)to induce microglial *** results suggest that inhibiting the interaction of Müller cells and microglia may attenuate microglial proliferation and migration in glaucoma.

关键词： Glaucoma chronic ocular hypertension Retinal microglia Proliferation Migration P2X7R/P2X4R Müller cells

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