检索结果-南通市图书馆

Protective effects of curcumin on retinal müller cell in early diabetic rats

International Journal of Ophthalmology(English edition) 2013年第4期6卷 422-424页

作者： Zhong-Fu Zuo Qiang Zhang Xue-Zheng Liu Department of Human Anatomy Liaoning Medical University

·AIm: To explore the effects and potential mechanisms of curcumin on retinal müller cell in early diabetic rats. ·mETHODS: Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (STZ). male Sprague-Dawley (SD) rats were randomly assigned into 4 groups: control group (nave SD rats administered with a single intraperitoneal injection of citric buffer), diabetic group (STZ -diabetic rats), dimethyl sulfoxide (DmSO) group (diabetic rats intraperitoneally administered with mixture of DmSO and normal saline, once a day) and curcumin group (diabetic rats intraperitoneally administered with curcumin, 80mg/kg, once a day). Three months after diabetes onset, malondialdehyde (mDA, indication of oxidative stress level) and reduced glutathione (GSH) in retina were detected with kits, glial fibrillary acidic protein (GFAP) in retina was revealed by immunohistochemistry and Western blot, and retinal glutamine synthetase (GS) were observed by Western blot. ·RESULTS: Compared with control group, retinal mDA was increased, and GSH was decreased in diabetic and DmSO groups ( mDA and GSH in curcumin group showed no difference compared with control group ( >0.05). Furthermore, upregulation of retinal GFAP and down-regulation of retinal GS were detected in diabetic and DmSO groups, and no alteration could be observed in curcumin group revealed with Western blot. Compared with control group, retinal müller cells showed significant increase in GFAP immunochemistry staining in diabetic and DmSO groups. moreover, GFAP -positive staining was decreased in curcumin group compared with diabetic group. · CONCLUSION: Curcumin inhibits diabetic retinal oxidative stress, protects müller cell, and prevents the down -regulation of GS in diabetic retina. Therefore, curcumin has a therapeutic potential in the treatment of diabetic retinopathy (DR).

关键词： diabetic retinopathy curcumin oxidative stress müller cell

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Paired Immunoglobulin-like Receptor B Inhibition in müller cells Promotes Neurite Regeneration After Retinal Ganglion cell Injury in vitro

引用

Neuroscience Bulletin 2020年第9期36卷 972-984页

作者： Rongdi Yuan mei Yang Wei Fan Jian Lan Yuan-Guo Zhou Department of Ophthalmology Xinqiao HospitalArmy Medical UniversityChongqing 400037China The molecular Biology Centre State Key Laboratory of TraumaBurn and Combined InjuryResearch Institute of Surgery and Daping HospitalArmy Medical UniversityChongqing 400042China

In the central nervous system(CNS),three types of myelin-associated inhibitors(mAIs) have major inhibitory effects on nerve regeneration.They include Nogo-A,myelin-associated glycoprotein,and oligodendrocyte-myelin glycoprotein.mAIs possess two co-receptors,Nogo receptor(NgR) and paired immunoglobulin-like receptor B(PirB).Previous studies have confirmed that the inhibition of NgR only results in a modest increase in regeneration in the CNS;however,the inhibitory effects of PirB with regard to nerve regeneration after binding to mAIs remain controversial.In this study,we demonstrated that PirB is expressed in primary cultures of retinal ganglion cells(RGCs),and the inhibitory effects of the three mAIs on the growth of RGC neurites are not significantly decreased after direct PirB knockdown using adenovirus PirB shRNA.Interestingly,we found that retinal müller cells expressed PirB and that its knockdown enhanced the regeneration of co-cultured RGC neurites.PirB knockdown also activated the JAK/Stat3 signaling pathway in müller cells and upregulated ciliary neurotrophic factor levels.These findings indicate that PirB plays a novel role in retinal müller cells and that its action in these cells may indirectly affect the growth of RGC neurites.The results also reveal that PirB in müller cells affects RGC neurite regeneration.Our findings provide a novel basis for the use of PirB as a target molecule to promote nerve regeneration.

关键词： Neurite regeneration müller cell Retina ganglion cell injury Ciliary neurotrophic factor

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Overexpressing NeuroD1 reprograms müller cells into various types of retinal neurons

引用

Neural Regeneration Research 2023年第5期18卷 1124-1131页

作者： Di Xu Li-Ting Zhong Hai-Yang Cheng Zeng-Qiang Wang Xiong-min Chen Ai-Ying Feng Wei-Yi Chen Gong Chen Ying Xu Guangdong-Hongkong-macao Institute of CNS Regeneration Key Laboratory of CNS Regeneration(Ministry of Education)Jinan UniversityGuangzhouGuangdong ProvinceChina Co-Innovation Center of Neuroregeneration Nantong UniversityNantongJiangsu ProvinceChina

The onset of retinal degenerative disease is often associated with neuronal loss. Therefore, how to regenerate new neurons to restore vision is an important issue. NeuroD1 is a neural transcription factor with the ability to reprogram brain astrocytes into neurons in vivo. Here, we demonstrate that in adult mice, NeuroD1 can reprogram müller cells, the principal glial cell type in the retina, to become retinal neurons. most strikingly, ectopic expression of NeuroD1 using two different viral vectors converted müller cells into different cell types. Specifically, AAV7 m8 GFAP681::GFP-ND1 converted müller cells into inner retinal neurons, including amacrine cells and ganglion cells. In contrast, AAV9 GFAP104::ND1-GFP converted müller cells into outer retinal neurons such as photoreceptors and horizontal cells, with higher conversion efficiency. Furthermore, we demonstrate that müller cell conversion induced by AAV9 GFAP104::ND1-GFP displayed clear dose-and time-dependence. These results indicate that müller cells in adult mice are highly plastic and can be reprogrammed into various subtypes of retinal neurons.

关键词： amacrine cell ganglion cell horizontal cell in vivo reprogramming müller cell NeuroD1 photoreceptor regeneration retina retinal degeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Osteopontin is a biomarker for early autoimmune uveoretinitis

引用

Neural Regeneration Research 2022年第7期17卷 1604-1608页

作者： Jeongtae Kim meejung Ahn Yuna Choi Jiyoon Chun Kyungsook Jung Akane Tanaka Hiroshi matsuda Taekyun Shin Department of Anatomy Kosin University College of MedicineBusanRepublic of Korea Department of Animal Science College of Life ScienceSangji UniversityWonjuRepublic of Korea Department of Veterinary Anatomy College of Veterinary Medicine and Veterinary Medical Research InstituteJeju National UniversityJejuRepublic of Korea Functional Biomaterials Research Center Korea Research Institute of Bioscience and BiotechnologyJeonbukRepublic of Korea Laboratory of Comparative Animal medicine Division of Animal Life ScienceInstitute of AgricultureTokyo University of Agriculture and TechnologyTokyoJapan

Osteopontin(OPN)is an extracellular matrix protein with a diverse range of functions,including roles in cell adhesion,migration,and immunomodulation,which are associated with the modulation of neuroinflammation in the central nervous system.The present study was performed to evaluate the involvement of OPN in the eyes of an experimental autoimmune uveoretinitis(EAU)model.The EAU model was developed by immunization of Lewis rats with interphotoreceptor retinoid-binding protein.The results showed the OPN level was remarkably upregulated in the eye of EAU rats on day 9 post-immunization.The level of CD44,a ligand of OPN,was increased in the ciliary body of EAU rats.Furthermore,OPN was also detected in the ciliary body and activated microglia/macrophages in the EAU retina.The results suggest that OPN was significantly upregulated in the eyes of EAU rats,and that it may be useful as an early biomarker of ocular autoimmune diseases.All animal experiments were approved by the Institutional Animal Care and Use Committee of Jeju National University(approval No.2020-0012)on march 11,2020.

关键词： CD44 ciliary body experimental autoimmune uveoretinitis macrophage müller cell osteopontin photoreceptor cell retina

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Dopamine D1 receptor-mediated upregulation of BKCa channels in retinal mller cell in a rat chronic ocular hypertension model

Dopamine D1 receptor-mediated upregulation of BKCa channels ...

引用

中国神经科学学会第十届全国学术会议

作者： Hang-Jing WU Yan-Ying mIAO min JI Wei YANG Xiong-Li YANG Zhong-Feng WANG Institutes of Brain Science Institute of Neurobiology and State Key Laboratory of Medical NeurobiologyFudan University

miiller cell gliosis is a universal response in many retinal pathological conditions.Our previous work demonstrated that downregulation of Kir K channels contributes to the miiller cells gliosis in a rat chronic ocular hypertension(COH) model.However,if and how outward K currents are involved in miiller cell gliosis in glaucoma are largely unknown.Here,we investigated the changes of TEA-sensitive large-conductance Ca-activated K(BK)channels in miiller cells in rat COH model reproduced by ligating three episcleral veins.We found that outward Kcurrent densities in miiller cells isolated from the COH rats were significantly increased.Further experiments showed that the increased outward K currents were mainly mediated by BK channels.The peak current densities of BKchannels were remarkably increased in miiller cells isolated from the COH rats during 1-4 weeks after the operation.Afterward,the current densities gradually declined to control level.We hypothesized that increased extracellular dopamine(DA) in glaucoma activates DA Dl receptors and then increases BK currents in miiller cells.In agreement with our hypothesis,SKF81297,a selective DA Dl receptor agonist,remarkably enhanced BK currents in miiller cells obtained from normal rats,and the effects were reversed by a Dl receptor antagonist SCH23390.Pretreatment with either Rp-cAmP,a competitive inhibitor of cAmP,or H-89,a PKA inhibitor,blocked SKF81297-induced effect on the BK while extracellular application of forskolin,an adenylate cyclase activator,mimicked the SKF81297 effect,suggesting an involvement of cAmP-PKA signaling pathway.Since increased BK currents may hyperpolarize the membrane potential of miiller cells,DA Dl receptor-mediated effect on BK of miiller cell in COH rats seems to oppose the Kir channel inhibition-induced depolarization of the cells,thereby attenuating miiller cell gliosis.

关键词： müller cell BKCa channel dopamine D1 receptor glaucoma

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Anti-VEGF therapy prevents müller intracellular edema by decreasing VEGF-A in diabetic retinopathy

引用

Eye and Vision 2021年第1期8卷 109-123页

作者： Tianqin Wang Chaoyang Zhang Hai Xie mengmeng Jiang Haibin Tian Lixia Lu Guo-Tong Xu Lin Liu Jingfa Zhang Department of Ophthalmology Renji HospitalShanghai Jiao Tong University School of Medicine160 Pujian RoadPudong New DistrictShanghai 200127China Department of Ophthalmology Shanghai General Hospital(Shanghai First People’s Hospital)Shanghai Jiao Tong University100 Haining RoadHongkou DistrictShanghai 200080China National Clinical Research Center for Eye Diseases Shanghai Key Laboratory of Ocular Fundus DiseasesShanghai Engineering Center for Visual Science and PhotomedicineShanghai Engineering Center for Precise Diagnosis and Treatment of Eye DiseasesShanghaiChina Tongji Eye Institute Tongji University School of Medicine1239 Siping RoadMedical School BuildingRoom 623Shanghai 200092China

Background:Although vascular endothelial growth factor A(VEGF-A)is known to play a key role in causing retinal edema,whether and how VEGF-A induces intracellular edema in the retina still remains unclear.methods:Sprague-Dawley rats were rendered diabetic with intraperitoneal injection of streptozotocin.Intravitreal injection of ranibizumab was performed 8 weeks after diabetes onset.rmC-1 cells(rat müller cell line)were treated with glyoxal for 24 h with or without ranibizumab.The expression levels of inwardly rectifying K^(+)channel 4.1(Kir4.1),aquaporin 4(AQP4),Dystrophin 71(Dp71),VEGF-A,glutamine synthetase(GS)and sodium-potassium-ATPase(Na^(+)-K^(+)-ATPase)were examined using Western blot.VEGF-A in the supernatant of the cell culture was detected with ELISA.The intracellular potassium and sodium levels were detected with specific indicators.Results:Compared with normal control,protein expressions of Kir4.1 and AQP4 were down-regulated significantly in diabetic rat retinas,which were prevented by ranibizumab.The above changes were recapitulated in vitro.Similarly,the intracellular potassium level in glyoxal-treated rmC-1 cells was increased,while the intracellular sodium level and Na^(+)-K^(+)-ATPase protein level remained unchanged,compared with control.However,ranibizumab treatment decreased intracellular sodium,but not potassium.Conclusion:Ranibizumab protected müller cells from diabetic intracellular edema through the up-regulation of Kir4.1 and AQP4 by directly binding VEGF-A.It also caused a reduction in intracellular osmotic pressure.

关键词： Diabetic retinopathy Diabetic macular edema müller cell Anti-VEGF Intracellular edema

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

PTEN knockdown with the Y444F mutant AAV2 vector promotes axonal regeneration in the adult optic nerve

引用

Neural Regeneration Research 2018年第1期13卷 135-144页

作者： Zheng-ru Huang Hai-ying Chen Zi-zhong Hu Ping Xie Qing-huai Liu Department of Ophthalmology the First Affiliated Hospital of Nanjing Medical University Nanjing Jiangsu Province China Department of Ophthalmology the Second People's Hospital of Changshu Changshu Jiangsu Province China

The lack of axonal regeneration is the major cause of vision loss after optic nerve injury in adult mammals. Activating the PI3K/AKT/mTOR signaling pathway has been shown to enhance the intrinsic growth capacity of neurons and to facilitate axonal regeneration in the central nervous system after injury. The deletion of the mTOR negative regulator phosphatase and tensin homolog （PTEN） enhances regeneration of adult corticospinal neurons and ganglion cells. In the present study, we used a tyrosine-mutated （Y444F） AAV2 vector to efficiently express a short hairpin RNA （shRNA） for silencing PTEN expression in retinal ganglion cells. We evaluated cell survival and axonal regeneration in a rat model of optic nerve axotomy. The rats received an intravitreal injection of wildtype AAV2 or Y444F mutant AAV2 （both carrying shRNA to PTEN） 4 weeks before optic nerve axotomy. Compared with the wildtype AAV2 vector, the Y444F mutant AAV2 vector enhanced retinal ganglia cell survival and stimulated axonal regeneration to a greater extent 6 weeks after axotomy. moreover,post-axotomy injection of the Y444F AAV2 vector expressing the shRNA to PTEN rescued ～19% of retinal ganglion cells and induced axons to regenerate near to the optic chiasm. Taken together, our results demonstrate that PTEN knockdown with the Y444F AAV2 vector promotes retinal ganglion cell survival and stimulates long-distance axonal regeneration after optic nerve axotomy. Therefore, the Y444F AAV2 vector might be a promising gene therapy tool for treating optic nerve injury.

关键词： nerve regeneration optic nerve axotomy gene therapy müller cell retinal ganglion cell AAV2 shRNA PTEN GLAST mTOR neural regeneration

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Absence of ephrin-A2/A3 increases retinal regenerative potential for müller cells in Rhodopsin knockout mice

引用

Neural Regeneration Research 2021年第7期16卷 1317-1322页

作者： Rui-Lin Zhu Yuan Fang Hong-Hua Yu Dong FChen Liu Yang Kin-Sang Cho Department of Ophthalmology Peking University First HospitalBeijingChina Schepens Eye Research Institute Massachusetts Eye and EarHarvard Medical SchoolBostonMAUSA Department of Ophthalmology and Visual Science Eye&ENT HospitalShanghai Medical CollegeFudan UniversityShanghaiChina Guangdong Eye Institute Department of OphthalmologyGuangdong Provincial People’s HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdong ProvinceChina

müller cells(mC) are considered dormant retinal progenitor cells in mammals.Previous studies demonstrated ephrin-As act as negative regulators of neural progenitor cells in the retina and brain.It remains unclear whether the lack of ephrin-A2/A3 is sufficient to promote the neurogenic potential of mC.Here we investigated whether the mC is the primary retinal cell type expressing ephrin-A2/A3 and their role on the neurogenic potential of müller cells.In this study, we showed that ephrin-A2/A3 and their receptor EphA4 were expressed in retina and especially enriched in mC.The level of ephrin As/EphA4 expression increased as the retina matured that is correlated with the reduced proliferative and progenitor cell potential of mC.Next, we investigated the proliferation in primary mC cultures isolated from wild-type and A2~(–/–) A3~(–/–) mice by 5-ethynyl-2′-deoxyuridine(EdU) incorporation.We detected a significant increase of EdU~+ cells in mC derived from A2~(–/–) A3~(–/–) mice.Next, we investigated the role of ephrin-A2/A3 in mice undergoing photoreceptor degeneration such as Rhodopsin knockout(Rho~(–/–)) mice.To further evaluate the role of ephrin-A2/A3 in mC proliferation in vivo, EdU was injected intraperitoneally to adult wild-type, A2~(–/–) A3~(–/–), Rho~(–/–) and Rho~(–/–) A2~(–/–) A3~(–/–) mice and the numbers of EdU~+ cells distributed among different layers of the retina.Ephrin As/EphA4 expression was upregulated in the retina of Rho~(–/–) mice compared to the wild-type mice.In addition, cultured mC derived from ephrin-A2~(–/–) A3~(–/–) mice also expressed higher levels of progenitor cell markers and exhibited higher proliferation potential than those from wild-type mice.Interestingly, we detected a significant increase of EdU~+ cells in the retinas of adult ephrin-A2~(–/–) A3~(–/–) mice mainly in the inner nuclear layer;and these EdU~+ cells were co-localized with mC marker, cellular retinaldehyde-binding protein, suggesting some proliferating cells are from mC.In Rhodopsin knockout mice(Rho~(–/–) A2~(–/–)

关键词： endogenous stem cell EphA4 ephrin-A2 ephrin-A3 ephrins müller cell photoreceptor cell regeneration retinal degeneration retinal regeneration retinal stem cell

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mechanism of the DL-alpha-aminoadipic acid inhibitory effect on form-deprived myopia in guinea pig

引用

International Journal of Ophthalmology(English edition) 2013年第1期6卷 19-22页

作者： Jun-Feng mao Shuang-Zhen Liu Department of Ophthalmology Xiangya Hospital of Central South University

AIm:To investigate the effect of intravitreal injection of DL-alpha-aminoadipic acid (DL-α-AAA) on ocular refractive state and retinal dopamine, transforming growth factor-β2 (TGFβ2 ), vasoactive intestinal polypeptide (VIP) in guinea pig form-deprived myopia. mETHODS:Four-week-old pigmented guinea pigs were randomly assigned to 4 groups:normal control, deprivation, deprivation plus DL-α-AAA, deprivation plus saline. Form deprivation was induced with the self-made translucent eye shields, and lasted for 14 days. 8μg DL-α-AAA was injected into the vitreous chamber of deprived eyes. The corneal radius of curvature, refraction and axial length were measured. Retinal dopamine content was evaluated by the high-performance liquid chromatography with electrochemical detection, and TGFβ2 and VIP protein were detected by Western blotting. RESULTS:Fourteen days of eye occlusion caused the axial length to elongate and become myopic in the form-deprived eyes, with the decrease of retinal dopamine and the increase of TGFβ 2 and vasoactive intestinal polypeptide (VIP) protein. Intravitreal injection of DL-α-AAA could inhibit the myopic shift from (-3.65±1.06)D to (-1.48 ±0.63)D, P mine and VIP protein in deprived eyes. Retinal TGFβ2 protein correlated highly with the ocular refraction (y =-3.34 + 0.31/x , F =74.75, P ment groups. ·CONCLUSION:Intravitreal injection of DL-α-AAA is effectively able to suppress the development of form deprivation myopia, which may be associated with retinalTGFβ2 protein in guinea pigs.

关键词： DL-alpha-aminoadipic acid form-deprivation myopia TGFβ2 müller cell retina

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：