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SIRT1 inhibits apoptosis of human lens epithelial cells through suppressing endoplasmic reticulum stress in vitro and in vivo

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International Journal of Ophthalmology(English edition) 2024年第7期17卷 1205-1216页

作者： Hui Cui Di Sun Sheng Meng Tian-Ju Ma Zi Ye Zhao-Hui Li Medical School of Chinese PLA Beijing 100089China Senior Department of Ophthalmology the Third Medical Center of PLA General HospitalBeijing 100853China

AIM:To explore the effect of silent information regulator factor 2-related enzyme 1(SIRT1)on modulating apoptosis of human lens epithelial cells(HLECs)and alleviating lens opacification of rats through suppressing endoplasmic reticulum(ER)stress.METHODS:HLECs(SRA01/04)were treated with varying concentrations of tunicamycin(TM)for 24h,and the expression of SIRT1 and C/EBP homologous protein(CHOP)was assessed using real-time quantitative polymerase chain reaction(RT-PCR),Western blotting,and immunofluorescence.Cell morphology and proliferation was evaluated using an inverted microscope and cell counting kit-8(CCK-8)assay,respectively.In the SRA01/04 cell apoptosis model,which underwent siRNA transfection for SIRT1 knockdown and SRT1720 treatment for its activation,the expression levels of SIRT1,CHOP,glucose regulated protein 78(GRP78),and activating transcription factor 4(ATF4)were examined.The potential reversal of SIRT1 knockdown effects by 4-phenyl butyric acid(4-PBA;an ER stress inhibitor)was investigated.In vivo,age-related cataract(ARC)rat models were induced by sodium selenite injection,and the protective role of SIRT1,activated by SRT1720 intraperitoneal injections,was evaluated through morphology observation,hematoxylin and eosin(H&E)staining,Western blotting,and RT-PCR.RESULTS:SIRT1 expression was downregulated in TMinduced SRA01/04 cells.Besides,in SRA01/04 cells,both cell apoptosis and CHOP expression increased with the rising doses of TM.ER stress was stimulated by TM,as evidenced by the increased GRP78 and ATF4 in the SRA01/04 cell apoptosis model.Inhibition of SIRT1 by siRNA knockdown increased ER stress activation,whereas SRT1720 treatment had opposite results.4-PBA partly reverse the adverse effect of SIRT1 knockdown on apoptosis.In vivo,SRT1720 attenuated the lens opacification and weakened the ER stress activation in ARC rat models.CONCLUSION:SIRT1 plays a protective role against TM-induced apoptosis in HLECs and slows the progression of cataract in rats by inhibiting ER stress.These findings sug

关键词： silent information regulator factor 2-related enzyme 1 endoplasmic reticulum stress apoptosis human lens epithelial cells cataract

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Role of reactive oxygen species in epithelial-mesenchymal transition and apoptosis of human lens epithelial cells

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International Journal of Ophthalmology(English edition) 2023年第12期16卷 1935-1941页

作者： Rui-Hua Jing Cong-Hui Hu Tian-Tian Qi Bo Ma Department of Ophthalmology the Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710004Shaanxi ProvinceChina Department of Ophthalmology the First Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710061Shaanxi ProvinceChina

AIM:To investigate the role of reactive oxygen species(ROS)in epithelial–mesenchymal transition(EMT)and apoptosis of human lens epithelial cells(HLECs).METHODS:Flow cytometry was used to assess ROS production after transforming growth factorβ2(TGF-β2)induction.Apoptosis of HLECs after H_(2)O_(2) and TGF-β2 interference with or without ROS scavenger N-acetylcysteine(NAC)were assessed by flow cytometry.The corresponding protein expression levels of the EMT markerα-smooth muscle actin(α-SMA),the extracellular matrix(ECM),marker fibronectin(Fn),and apoptosis-associated proteins were detected by using Western blotting in the presence of an ROS scavenger(NAC).Wound-healing and Transwell assays were used to assess the migration capability of HLECs.RESULTS:TGF-β2 stimulates ROS production within 8h in HLECs.Additionally,TGF-β2 induced HLECs cell apoptosis,EMT/ECM synthesis protein markers expression,and pro-apoptotic proteins production;nonetheless,NAC treatment prevented these responses.Similarly,TGF-β2 promoted HLECs cell migration,whereas NAC inhibited cell migration.We further determined that although ROS initiated apoptosis,it only induced the accumulation of the EMT markerα-SMA protein,but not COL-1 or Fn.CONCLUSION:ROS contribute to TGF-β2-induced EMT/ECM synthesis and cell apoptosis of HLECs;however,ROS alone are not sufficient for EMT/ECM synthesis.

关键词： human lens epithelial cells epithelial-mesenchymal transition transforming growth factorβ2 reactive oxygen species apoptosis

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Parthenolide protects human lens epithelial cells from oxidative stress-induced apoptosis via inhibition of activation of caspase-3 and caspase-9

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Cell Research 2007年第6期17卷 565-571页

作者： Hangping YaoXiajing TangXueting ShaoLei FengNanping WuKe YaoNational Key Laboratory of Infectious Diseases, Institute of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, ChinaEye Center, Second Affiliated Hospital School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou 310009, China National Key Laboratory of Infectious Diseases Institute of Infectious Diseases First Affiliated Hospital School of Medicine Zhejiang University Hangzhou China Eye Center Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou China

The apoptosis of lens epithelial cells has been proposed as the common basis of cataract formation, with oxidative stressas the major cause. This study was performed to investigate the protective effect of the herbal constituent parthenolideagainst oxidative stress-induced apoptosis of human lens epithelial （HLE） cells and the possible molecular mechanismsinvolved. HLE cells （SRA01-04） were incubated with 50μM H2O2 in the absence or presence of different doses ofparthenolide （10, 20 and 50μM）. To study apoptosis, the cells were assessed by morphologic examination and AnnexinV-propidium iodide double staining flow cytometry; to investigate the underlying molecular mechanisms, the expressionof caspase-3 and caspase-9 were assayed by Western blot and quantitative RT-PCR, and the activities of caspase-3 andcaspase-9 were measured by a Chemicon caspase colorimetric activity assay kit. Stimulated with H2O2 for 18 h, a highfraction of HLE cells underwent apoptosis, while in the presence of parthenolide of different concentrations, dose-depen-dent blocking of HLE cell apoptosis was observed. The expression of caspase-3 and caspase-9 induced by H2O2 in HLEcells was significantly reduced by parthenolide both at the protein and mRNA levels, and the activation of caspase-3 andcaspase-9 was also suppressed by parthenolide in a dose-dependent manner. In conclusion, parthenolide prevents HLEcells from oxidative stress-induced apoptosis through inhibition of the activation of caspase-3 and caspase-9, suggestinga potential protective effect against cataract formation.

关键词： parthenolide human lens epithelial cells apoptosis caspase-3 and caspase-9

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MicroRNA-34a promoting apoptosis of human lens epithelial cells through down-regulation of B-cell lymphoma-2 and silent information regulator

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International Journal of Ophthalmology(English edition) 2016年第11期9卷 1555-1560页

作者： Qing-Lan Li Hong-Yang Zhang Yong-Jie Qin Qian-Li Meng Xiao-Lei Yao Hai-Ke Guo Department of Ophthalmology Ruikang Hospital affiliated to Guangxi University of Chinese Medicine Department of Ophthalmology Guangdong General Hospital and Guangdong Academy of Medical Sciences Zhengzhou Aier Eye Hospital Aier School of OphthalmologyCentral South University

AIM： To investigate the role of micro RNA-34a（mi R-34a） in the induction of apoptosis of human lens epithelial（HLE-B3） cells. METHODS： The apoptosis of HLE-B3 cells was detected by Annexin V-PE apoptosis detection kit after the treatment with 200 μmol/L H2O2 for 24h and lentiviral mi R-34 a vector transfection. The expression of mi R-34 a in the cells was quantified by quantitative real time polymerase chain reaction（q RT-PCR） in response to H2O2 exposure and the vector transfection. The effects of overexpression of mi R-34 a on the expression of B-cell lymphoma-2（Bcl-2） and silent information regulator 1（SIRT1） was determined by q RT-PCR and Western blot. RESULTS： The expression of mi R-34 a was up-regulated by the treatment of H2O2 in HLE-B3 cells. The increased expression of mi R-34 a is accompanied with the cell apoptosis. Consistence with the H2O2 exposure,ectopic overexpression of mi R-34 a in HLE-B3 cells promoted cells apoptosis. Importantly the anti-apoptosis factors Bcl-2 and SIRT1 were reduced significantly by up-regulation of mi R-34 a in HLE-B3 cells.CONCLUSION： Mi R-34 a promotes the apoptosis of HLE-B3 cells by down-regulating Bcl-2 and SIRT1,suggesting that mi R-34 a may involve in the pathogenesis of cataract formation and targeting mi R-34 a may be a potentially therapeutic approach for treatment of cataract.

关键词： human lens epithelial cells microRNA-34a apoptosis

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Effects of Mitogen-activated Protein Kinase Signal Pathway on Heat Shock Protein 27 Expression in human lens epithelial cells Exposed to Sodium Salicylate in vitro

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第3期29卷 377-382页

作者：王智高瑞莹黄渝侃田博周龑莉 Deppartment of Ophthalmology Union Hospital of Tongji Medical College Huazhong University of Science and Technology Aier Eye Hospital

The roles of mitogen-activated protein kinase （MAPK） signal pathway in sodium salieylate-induced expression of heat shock protein 27 （HSP27） in human lens epithelial cells （HLECs-B3） in vitro were investigated. HLECs-B3 were incubated in the fresh media containing sodium salicylate at different concentrations for different durations, and allowed to be recovered in fresh medium without sodium salicylate for different durations with or without pretreatment with p38MAPK inhibitor （SB203580）, ERK1/2 inhibitor （PD98059） and JNK/SAPK inhibitor （SP600125）. The expression of P38MAPK, ERK1/2, JNK/SAPK, phosphorylated P38MAPK, phosphorylated ERK1/2, phosphorylated JNK/SAPK and HSP27 was detected by Western blot. The expression of HSP27 mRNA and protein was detected by RT-PCR and immunohistochemistry respectively. It was found there was only weak expression of HSP27 in normal HLECs. The expression of HSP27 was not detectable in HLECs-B3 that were exposed to sodium salicylate （55 retool/L） for 1-5 h. It was indicated that recovery from sodium salicylate （〉35 mmol/L） significantly increased the synthesis of HSP27. The expression of HSP27 was up-regulated in HLECs-B3 under sodium salicylate recovery for 3 h, reached the peak level for 6 h, and returned to the level of control cells by 24 h. Activation of P38MAPK from sodium salicylate stimulation occurred at 30th rain, and increased significantly at 1st h, then declined and renamed to baseline level at 3rd h under sodium salicylate recovery. Activation of ERK1/2 occurred at 1st h and reached the peak level at 6th h under sodium salicylate recovery. However, JNK/SAPK was inactivated by sodium salicylate. The expression of HSP27 could be down-regulated with the pretreatment of SB203580 and PD98059 jointly. It is concluded that sodium salicylate can induce the expression of HSP27 in HLECs-B3. The effects are mediated, at least in part, through the activation of P38MAPK and ERK1/2 signaling pathway.

关键词： sodium salicylate human lens epithelial cells mitogen-activated protein kinase heat shock protein

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Effects of lentiviral RNA interference-mediated downregulation of integrin-linked kinase on biological behaviors of human lens epithelial cells

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International Journal of Ophthalmology(English edition) 2016年第1期9卷 21-28页

作者： Yu-Ping Zheng Shao-Bo Zhang Feng Wang Hui Liu Wen Zhang Bin Song Zi-Yao Liu Lei Xiong Ya-Zhi Fan Ding-Ying Liao Department of Ophthalmology the Second Affiliated Hospital School of Medicine Xi'an Jiaotong University Department of Ophthalmology Tangdu Hospital the Fourth Military Medical University Department of Otolaryngology Shaanxi Provincial People's Hospital

AIM：To investigate the effects of lentivirus（LV）mediated integrin-linked kinase（ILK）RNA interference（RNAi）on biological behaviors of human lens epithelial cells（LECs）.·METHODS：human cataract LECs and immortalized human LEC line,human lens epithelial（HLE）B-3 cells were transfected by lentiviral vector expressing ILKspecific short hairpin RNA（sh RNA）and then stimulated by transforming growth factor-β（TGF-β）,the silencing of ILK gene and protein was identified by reverse transcription-polymerase chain reaction（RT-PCR）and Western blot methods;biological behaviors including cell cycle and apoptosis,cell morphology,α-smooth muscle actin（SMA）stress fiber formation and cell migration were examined.·RESULTS：Remarkable decreases of ILK protein expression were detected in LECs carrying lentiviral ILK-sh RNA vector;flow cytometry revealed arresting of cell cycle progression through the G1/S transition and higher apoptosis rate in ILK-RNAi-LV transfected cells.Lessα-SMA stress fiber formation and migration was observed in ILK-RNAi-LV transfected LECs.·CONCLUSION：The present study demonstrated that ILK was an important regulator for LECs proliferation and migration.LV mediated ILK RNAi is an effective way todecrease ILK-regulated cell growth by arresting cell cycle progression and increasing cell apoptosis,as well as,to prevent cell migration by inhibiting TGF-βinducedα-SMA stress fiber formation.Thus,LV mediated ILK RNAi might be useful to prevent posterior capsular opacification.

关键词： human lens epithelial cells integrin-linkedkinase RNA interference Lentivirus posterior capsularopacification

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In vitro inhibition of proliferation,migration and epithelial-mesenchymal transition of human lens epithelial cells by fasudil

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International Journal of Ophthalmology(English edition) 2018年第8期11卷 1253-1257页

作者： Jing-Zhi Shao Ying Qi Shan-Shan Du Wen-Wen Du Fu-Zhen Li Feng-Yan Zhang Department of Ophthalmology the First Affiliated Hospital of Zhengzhou University

AIM： To study the potential role of fasudil as a treatment for posterior capsular opacification（PCO） of the human crystalline lens.METHODS： human lens epithelial cells（HLECs; line SRA01/04） was exposed to transforming growth factor-β2（TGF-β2） to induce the process of epithelial-mesenchymal transition（EMT）. Fasudil was applied to the cell samples. Its effect on overall HLECs proliferation and migration was studied, as was its influence on EMT induction by TGF-β2 using cell migration assay, MTT colorimetric assay and Western blot assay.RESULTS： Fasudil inhibited the proliferation of SRA01/04. Its effect was time-and concentration-dependent. The migration of SRA01/04 cells was significantly reduced 24-72 h after fasudil treatment, and the half maximal inhibitory concentration（IC50） was 22.37 μmol/mL at 72 h. Reversal of the elongated, fibroblast-like shape changes induced by TGF-β2 in SRA01/04 cells was observed. Fasudil up-regulated the expression of Connexin43 protein and down-regulated the expression of α-SMA protein compared with the cells treated with TGF-β2. Furthermore, when exposed to fasudil, the phosphorylation of Rhoassociated protein kinase（Rock） and myosin light chain（MLC） could not be activated in the cell preparations.CONCLUSION： Fasudil suppresses the proliferation and migration of SRA01/04 cells, and inhibits the process of EMT induced by TGF-β2. These results suggest that fasudil may serve as a therapeutic agent for PCO.

关键词： fasudil human lens epithelial cells TGF-β2 Rho/Rock epithelial-mesenchymal transition

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Effects of Sodium Salicylate on the Expression of HSP27 Protein during Oxidative Stress in Tissue-cultured human lens epithelial cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2006年第6期26卷 753-755页

作者：王智周莉 Department of Ophthalmology Union Hospital Tongji Medical College Huazhong University of Science and Technology

The effects of sodium salicylate on the expression of heat shock protein 27 （HSP27） during oxidative stress in tissue-cultured human lens epithelial cells were investigated. Cultured human lens epithelial cells （HLB-3） were divided into 3 groups： control group （group A）, oxidation injury group （group B） and sodium salicylate group （group C）. Apoptosis of human lens epithelial cells cultured in vitro was induced in the presence of 150 μmol/L H2O2. cells viability and the expression of HSP27 were analyzed. Viability of the cells was measured by methyl thiazole tetrazolium （MTT） chromatometry. The expression of HSP27 in HLB-3 cells was detected by using immunohistochemistry and image analysis system, Sodium salicylate could induce the expression of HSP27, and the cells viability in group C was significantly higher than in group B （0.2667±0.01414 vs 0.2150±0.01080, P=0.012〈0.05）. The average gray value of HSP27 in group B was less than that in group C （P=0.000〈0.05）. The increased expression of HSP27 by sodium salicylate might play an important role in the protection of hydrogen peroxide-induced injury of human lens epithelial cells, suggesting that sodium salicylate could suppress, at least in part, the apoptosis of human lens epithelial cells.

关键词： apoptosis human lens epithelial cells heat shock protein 27 sodium salicylate hydrogen peroxide

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Alu antisense RNA ameliorates methylglyoxal-induced human lens epithelial cell apoptosis by enhancing antioxidant defense

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International Journal of Ophthalmology(English edition) 2023年第2期16卷 178-190页

作者： Pei-Yuan Wu Ning Ji Chong-Guang Wu Xiao-Die Wang Xin Liu Zhi-Xue Song Murad Khan Suleman Shah Ying-Hua Du Xiu-Fang Wang Li-Fang Yan Department of Genetics Hebei Medical UniversityHebei Key Lab of Laboratory AnimalShijiazhuang 050017Hebei ProvinceChina Department of Ophthalmology Beijing Tiantan HospitalCapital Medical UniversityBeijing 100070China

AIM:To determine whether an antisense RNA corresponding to the human Alu transposable element(Aluas RNA)can protect human lens epithelial cells(HLECs)from methylglyoxal-induced apoptosis.METHODS:Cell counting kit-8(CCK-8)and 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assays were used to assess HLEC viability.HLEC viability/death was detected using a Calcein-AM/PI double staining kit;the annexin V-FITC method was used to detect HLEC apoptosis.The cytosolic reactive oxygen species(ROS)levels in HLECs were determined using a reactive species assay kit.The levels of malondialdehyde(MDA)and the antioxidant activities of total-superoxide dismutase(T-SOD)and glutathione peroxidase(GSH-Px)were assessed in HLECs using their respective kits.RT-q PCR and Western blotting were used to measure m RNA and protein expression levels of the genes.RESULTS:Aluas RNA rescued methylglyoxal-induced apoptosis in HLECs and ameliorated both the methylglyoxalinduced decrease in Bcl-2 m RNA and the methylglyoxalinduced increase in Bax m RNA.In addition,Aluas RNA inhibited the methylglyoxal-induced increase in Alu sense RNA expression.Aluas RNA inhibited the production of ROS induced by methylglyoxal,restored T-SOD and GSHPx activity,and moderated the increase in MDA content after treatment with methylglyoxal.Aluas RNA significantly restored the methylglyoxal-induced down-regulation of Nrf2 gene and antioxidant defense genes,including glutathione peroxidase,heme oxygenase 1,γ-glutamylcysteine synthetase and quinone oxidoreductase 1.Aluas RNA ameliorated methylglyoxal-induced increases of the m RNA and protein expression of Keap1 that is the negative regulator of Nrf2.CONCLUSION:Aluas RNA reduces apoptosis induced by methylglyoxal by enhancing antioxidant defense.

关键词： human Alu antisense RNA human lens epithelial cells methylglyoxal toxicity antioxidant defense apoptosis

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Effect of nano-selenium loaded with lycium barbarum polysaccharide on the proliferation of lens epithelial cells after UVB damage in vitro

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International Journal of Ophthalmology(English edition) 2022年第1期15卷 9-14页

作者： Jing-Xiang Zhong Shan-Shan Jin Kang-Sheng Wu Guo-Cheng Yu Lei-Lei Tu Lian Liu Department of Ophthalmology the First Affiliated Hospital of Jinan UniversityGuangzhou 510630Guangdong ProvinceChina

AIM:To investigate the effect of nano-selenium loaded with different concentrations of lycium barbarum polysaccharide(LBP-Se NPs)on the proliferation of human lens epithelial cells(HLECs)from UV irradiation.METHODS:LBP-Se NPs were prepared and their particle size was detected.HLECs(SRA01/04)were irradiated with UVB for different time(0,10,20,30,40,50,60 min)to construct a damaged model,the survival rate of cells was determined by methylthiazol tetrazolium(MTT)assay.The 4’,6-Diamidine-2’-phenylindole dihydrochloride(DAPI)staining was used to observe the status of cell nucleus and drug entering cytoplasm through cell membrane in SRA01/04 cells after adding LBP-SENPS loaded with coumarin fluorescence agent 24 h under fluorescence microscope.SRA01/04 normal and UVB-damaged cells were treated with different amounts of LBP-Se NPs at different concentrations,cells proliferation were observed.RESULTS:The particle size of LBP-Se NPs was stable in the range of 150-200 nm.The survival rate changes with time after UVB irradiation were statistically significant.The 10 min of UVB exposure as the time was chosen to construct the cell damage model.With DAPI staining,LBPSe NPs were observed to enter the cytoplasm through the cell membrane under fluorescence inverted microscope.Cytotoxicity of SRA01/04 at different concentrations of LBPSe NPs were measured.Cell survival rate was statistically different compared with the control group.The higher the loading concentration of LBP in nano-Se drugs was,the higher the cell proliferation rate was(Pcells appeared more cytoplasm dehydration,cell shrinkage and apoptotic bodies,and cell density decreased.CONCLU

关键词： lycium barbarum polysaccharide nano-selenium human lens epithelial cells ultraviolet irradiation

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