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akt2抑制剂促进大鼠根尖周炎症微环境中巨噬细胞的极化:基于降低miR-155-5p的表达

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南方医科大学学报 2023年第4期43卷 568-576页

作者：李敬怡杨思圆韩振江天乐朱耀周子航周静萍皖南医学院口腔医学院//皖南医学院口腔疾病研究中心安徽芜湖241000

目的通过构建大鼠慢性根尖周炎模型,探讨akt2抑制剂对根尖周组织巨噬细胞极化的影响及其相关因素。方法随机选取32只健康SD大鼠,其中28只作为实验组,通过髓腔开放法建立大鼠根尖周炎模型,在模型构建过程中分别在下颌第一磨牙左右侧髓腔... 详细信息

目的通过构建大鼠慢性根尖周炎模型,探讨akt2抑制剂对根尖周组织巨噬细胞极化的影响及其相关因素。方法随机选取32只健康SD大鼠,其中28只作为实验组,通过髓腔开放法建立大鼠根尖周炎模型,在模型构建过程中分别在下颌第一磨牙左右侧髓腔内注射生理盐水和akt2抑制剂。另外4只为健康对照组,不做任何处理。于开髓后第7、14、21、28天随机处死7只实验组和1只健康对照组大鼠后,分离下颌骨获取样本。X线和苏木精-伊红(HE)染色观察根尖周组织炎症浸润情况;免疫组织化学(IHC)染色观察akt2、巨噬细胞及炎症介质的表达与定位,逆转录-聚合酶链反应(RT-PCR)观察akt2、CD86、CD163、炎症介质(IL-6、IL-10)、miR-155-5p及C/EBPβ的mRNA表达,分析对巨噬细胞极化的影响。结果X线和苏木精-伊红染色结果显示:髓腔开放21 d后大鼠根尖周表现明显的慢性炎症,确认慢性大鼠根尖周炎模型构建成功。IHC染色和RT-PCR结果表明:与健康对照组相比,髓腔开放21 d后实验组大鼠根尖周炎组织中akt2、CD86、CD163、miR-155-5p、C/EBPβ、及IL-10表达显著增高(Pakt2抑制剂组大鼠根尖周组织中akt2、CD86、miR-155-5p和IL-6的表达水平以及CD86+M1型/CD163+M2型巨噬细胞比值显著降低(Pakt2可减缓大鼠根尖周炎症进展,促进大鼠根尖周炎症微环境中巨噬细胞向M2型极化;akt2抑制剂可能通过降低miR-155-5p表达,激活akt信号通路中转录因子C/EBPβ的表达,从而影响巨噬细胞极化。

关键词：根尖周炎 akt2 巨噬细胞极化 miR-155-5p C/EBPβ

Ablation of akt2 and AMPKα2 rescues high fat diet-induced obesity and hepatic steatosis through Parkin-mediated mitophagy

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Acta Pharmaceutica Sinica B 2021年第11期11卷 3508-3526页

作者： Shuyi Wang Jun Tao Huaguo Chen Machender R.Kandadi Mingming Sun Haixia Xu Gary D.Lopaschuk Yan Lu Junmeng Zheng Hu Peng Jun Ren Department of Emergency Shanghai Tenth People's HospitalSchool of Medicine Tongji UniversityShanghai 200072China Shanghai University School of Medicine Shanghai 200044China University of Wyoming College of Health Sciences LaramieWY 82071USA Department of Cardiovascular Surgery Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510000China Medprime Health Services LLC ParisTX 75460USA Department of Cardiology Shanghai Institute of Cardiovascular DiseasesZhongshan Hospital Fudan UniversityShanghai 200032China Department of Cardiology Affiliated Hospital of Nantong UniversityNantong 226001China Cardiovascular Research Centre University of AlbertaEdmontonAlberta T6G 2S2Canada Key Laboratory of Metabolism and Molecular Medicine Ministry of EducationDepartment of Endocrinology and MetabolismZhongshan Hospital Fudan UniversityShanghai 200032China Department of Laboratory Medicine and Pathology University of WashingtonSeattleWA 98195USA

Given the opposing effects of akt and AMP-activated protein kinase(AMPK)on metabolic homeostasis,this study examined the effects of deletion of akt2 and AMPKα2 on fat diet-induced hepatic steatosis.akt2–Ampkα2 double knockout(DKO)mice were placed on high fat diet for 5 months.Glucose metabolism,energy homeostasis,cardiac function,lipid accumulation,and hepatic steatosis were examined.DKO mice were lean without anthropometric defects.High fat intake led to adiposity and decreased respiratory exchange ratio(RER)in wild-type(WT)mice,which were ablated in DKO but not akt2^(-/-) and Ampkα2^(-/-) mice.High fat intake increased blood and hepatic triglycerides and cholesterol,promoted hepatic steatosis and injury in WT mice.These effects were eliminated in DKO but not akt2^(-/-) and Ampkα2^(-/-) mice.Fat diet promoted fat accumulation,and enlarged adipocyte size,the effect was negated in DKO mice.Fat intake elevated fatty acid synthase(FAS),carbohydrate-responsive element-binding protein(CHREBP),sterol regulatory element-binding protein 1(SREBP1),peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PGC-1α),peroxisome proliferator-activated receptor-α(PPARα),PPARγ,stearoyl-CoA desaturase 1(SCD-1),phosphoenolpyruvate carboxykinase(PEPCK),glucose 6-phosphatase(G6Pase),and diglyceride O-acyltransferase 1(DGAT1),the effect was absent in DKO but not akt2^(-/-) and Ampkα2^(-/-) mice.Fat diet dampened mitophagy,promoted inflammation and phosphorylation of forkhead box protein O1(FoxO1)and AMPKα1(Ser^(485)),the effects were eradicated by DKO.Deletion of Parkin effectively nullified DKO-induced metabolic benefits against high fat intake.Liver samples from obese humans displayed lowered microtubule-associated proteins 1A/1B light chain 3B(LC3B),Pink1,Parkin,as well as enhanced phosphorylation of akt,AMPK(Ser^(485)),and FoxO1,which were consolidated by RNA sequencing(RNAseq)and mass spectrometry analyses from rodent and human livers.These data suggest that concurrent deletion of akt2 and AMPKα2 offers resilience to f

关键词： akt2 AMPK Parkin High fat intake Obesity Steatosis Mitophagy FoxO1

Effect of Spindle Checkpoint on akt2-mediated Paclitaxel-resistance in A2780 Ovarian Cancer Cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第2期30卷 206-211页

作者：周婷鲍引娣叶双梅翁丹卉陈刚卢运萍马丁王世宣 Cancer Biology Research Center Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology

Recent evidence has suggested that akt2 plays an important role in the protection of cells from paclitaxel （PTX）-induced apoptosis and control of the cell cycle. In addition, some scholars suggested that the PTX sensitivity depends on a functional spindle assembly checkpoint. In the present study, we investigated the role of the akt2/Bubl cross-talking in apoptosis and cell cycle after exposure of the A2780 ovarian cancer cells to paclitaxel （PTX）. Recombinant expression plasmid WT-akt2 was transfected into A2780 cells by lipofectamine2000, and then the expression level of akt2 gene was detected by using RT-PCR and Western blotting. Cell apoptosis and cell cycle were detected by flow cytometry and Hoechst 33342 staining after treatment with PTX. Moreover, we compared the expression level of Bubl in different groups by Western blotting. Our study showed that up-regulation of akt2 contributed to A2780 ovarian cancer cells overriding PTX-induced G2/M arrest, and inhibited Bubl expression. Our findings might shed light on the molecular mechanism of PTX-induced resistance in ovarian cancer and help develop novel anti-neoplastic strategies.

关键词： resistance paclitaxel ovarian cancer cells akt2 spindle checkpoint

MicroRNA-194 inactivates hepatic stellate cells and alleviates liver fibrosis by inhibiting akt2

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World Journal of Gastroenterology 2019年第31期25卷 4468-4480页

作者： Jun-Cheng Wu Rong Chen Xin Luo Zheng-Hong Li Sheng-Zheng Luo Ming-Yi Xu Department of Gastroenterology Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghai 200080China Shanghai Key Laboratory of Pancreatic Diseases Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghai 200080China

BACKGROUND Activation of hepatic stellate cells(HSCs)is a pivotal event in the onset and progression of liver fibrosis.Loss of microRNA-194(miR-194)has been reported in activated HSCs,but the actual role of miR-194 in liver fibrosis remains uncertain.AIM To explore the role and potential mechanism of miR-194-mediated regulation of liver fibrosis in vitro and in vivo.METHODS The expression of miR-194 was examined in human fibrotic liver tissues,activated HSCs,and a carbon tetrachloride(CCl4)mouse model by qPCR.The effects of akt2 regulation by miR-194 on the activation and proliferation of HSCs were assessed in vitro.For in vivo experiments,we reintroduced miR-194 in mice using a miR-194 agomir to investigate the functions of miR-194 in liver fibrosis.RESULTS MiR-194 expression was notably lacking in activated HSCs from both humans and mice.Overexpression of miR-194(OV-miR-194)inhibitedα-smooth muscle actin(α-SMA)and type I collagen(Col I)expression and suppressed cell proliferation in HSCs by causing cell cycle arrest in G0/G1 phase.akt2 was predicted to be a target of miR-194.Notably,the effects of miR-194 knockdown in HSCs were almost blocked by akt2 deletion,indicating that miR-194 plays a role in HSCs via regulation of akt2.Finally,miR-194 agomir treatment dramatically ameliorated liver fibrosis in CCl4-treated mice.CONCLUSION We revealed that miR-194 plays a protective role by inhibiting the activation and proliferation of HSCs via akt2 suppression.Our results further propose miR-194 as a potential therapeutic target for liver fibrosis.

关键词： Hepatic stellate cells Liver fibrosis MicroRNA-194 akt2

akt2及磷酸化akt2在非小细胞肺癌中的表达及临床意义

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四川大学学报（医学版） 2010年第4期41卷 586-589页

作者：蒲蓉李为民刘丹莫显明唐颖刘伦旭陈渤江四川大学华西医院呼吸内科成都610041 四川大学华西医院生物治疗国家重点实验室干细胞生物研究室成都610041 四川大学华西医院病理科成都610041 四川大学华西医院胸心外科成都610041

目的研究akt2及磷酸化akt2(p-akt2)在非小细胞肺癌(NSCLC)组织中的表达及临床意义。方法应用免疫组织化学法检测137例非小细胞肺癌组织中akt2和p-akt2表达,分析akt2及p-akt2表达与肺癌预后的关系。结果非小细胞肺癌组织中akt2在腺癌及... 详细信息

目的研究akt2及磷酸化akt2(p-akt2)在非小细胞肺癌(NSCLC)组织中的表达及临床意义。方法应用免疫组织化学法检测137例非小细胞肺癌组织中akt2和p-akt2表达,分析akt2及p-akt2表达与肺癌预后的关系。结果非小细胞肺癌组织中akt2在腺癌及鳞癌组织中的阳性表达率分别为60.5%和54.1%,差异无统计学意义(P>0.05);p-akt2在腺癌及鳞癌组织中的阳性表达率分别为68.4%和47.5%,差异有统计学意义(Pakt2和p-akt2的表达在患者的年龄、性别、肿瘤TNM分期及细胞分化程度等方面差异无统计学意义(P>0.05)。生存分析显示,akt2表达阳性的NSCLC患者5年生存率及中位生存时间与阴性表达者比较差异无统计学意义〔36%vs.30%,(33.960±2.485)月vs.(31.338±2.868)月,P>0.05〕;而p-akt2表达阳性的患者5年生存率及中位生存时间与阴性表达者比较差异有统计学意义〔20%vs.56%,(28.464±2.235)月vs.(39.214±3.075)月,Pakt2表达阳性者5年中位生存时间与阴性表达者比较差异无统计学意义〔(34.778±4.469)月vs.(40.133±5.632)月,P>0.05〕;而p-akt2表达阳性的NSCLC患者5年中位生存时间与阴性表达者比较差异有统计学意义〔(29.808±4.337)月vs.(47.875±4.852)月,Pakt2在肺腺癌中的表达高于肺鳞癌,且p-akt2的阳性表达缩短了NSCLC患者的5年中位生存时间。

关键词： akt2 磷酸化akt2 非小细胞肺癌

反义及显性负调节akt2 RNA对脑胶质瘤细胞增殖抑制作用的体外研究

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癌症 2004年第11期23卷 1267-1272页

作者：康春生浦佩玉李捷王广秀天津医科大学总医院神经外科天津市神经病学研究所神经肿瘤实验室天津300052

背景与目的:表皮生长因子受体(epidermalgrowthfactorreceptor,EGFR)下游的丝苏氨酸激酶2(serine/threoninekinase2,akt2)信号转导通路对肿瘤细胞的生存和凋亡具有十分重要的作用。本文研究了反义akt2(antisenseakt2,AS-akt2)和显性负调节akt2(dominant-negativeakt2,DN-akt2)构建体对人脑胶质瘤细胞系TJ905的增殖和凋亡的调控作用。方法:脂质体介导akt2构建体转染人脑胶质瘤细胞系TJ905,原位杂交和蛋白印迹法检查akt2的表达水平,Ki-67标记指数和MTT法检测细胞增殖能力,TUNEL法计算凋亡指数评价肿瘤细胞凋亡的变化。结果:对每种akt2构建体转染后随机选择3个扩增后进一步分析。原位杂交和蛋白印迹结果表明,转染AS-akt2后akt2表达显著抑制,转染DN-akt2后akt2表达无明显变化。MTT研究发现:AS-akt2组和DN-akt2组的6天细胞生存率分别为(49.30～51.46)%和(50.52～55.23)%,细胞存活率显著低于对照组和空载体组(Pakt2组和DN-akt2组的标记指数(Ki-67labelingindex,Ki-67LI)分别为(57.50～59.33)%和(59.17～61.00)%,明显低于对照组(76.50%)和空载体组(74.83%)(Pakt2组(8.33%～8.83%)和DN-akt2组(7.50%～7.83%)

关键词：胶质瘤 akt2 反义及显性负调节akt2 转染增殖凋亡

Suppression of Glioma-Cell Survival by Antisense and Dominant-Negative akt2 RNA

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Chinese Journal of Clinical Oncology 2005年第3期2卷 609-614页

作者： PeiyuPu ChunshengKang JieLi GuangxiuWang DepartmentofNeurosurgery TianjinMedicalUniversityGeneralHospitalLaboratoryofNeuro-oncologyTianjinNeurologicalInstituteTianjin300052China

OBJECTIVE Overexpression of growth factors and their receptors such as PDGF, FGF, VEGF, IGF, EGF, TGFα etc. play a critical role in the development and progression of malignant gliomas. akt, one of the most potent downstream signaling effectors of these growth factor receptors is usually overactivated in malignant gliomas. The present study was undertaken to investigate the effects of antisense and dominant negative akt2 RNA on the survival of glioma cells with overexpression of akt2. METHODS Antisense and dominant negative akt2 constructs (AS-akt2, DN-akt2) were transfected into human glioblastoma cell line T J905 with overexpression of akt2. Using Western blotting, MTT assay, Ki67 labeling index (Ki67 LI), flow cytometry and the TUNEL method, the expression of akt2 and GFAP, the proliferation rate and apoptosis of glioma cells transfected with AS-akt2 or DN-akt2 were compared to those characteristics of parental and glioma cells transfected with an empty vector. RESULTS Cell proliferation was inhibited in glioma cells transfected with ASakt2 and DN-akt2 RNA, while GFAP expression and apoptosis were markedly increased in those cells. CONCLUSION akt is an important mediator in the growth signaling pathway of malignant gliomas and is a potential promising therapeutic target for malignant gliomas.

关键词：神经胶质瘤肿瘤细胞 akt2 RNA 基因表达

低氧肿瘤微环境通过akt-PDK1-YKL40通路诱导非小细胞肺癌侵袭性生长和血管生成

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低氧肿瘤微环境通过Akt-PDK1-YKL40通路诱导非小细胞肺癌侵袭性生...

作者：王伟中国人民解放军海军军医大学

学位级别：硕士

研究目的肺癌的恶性转移和复发是临床治疗过程中经常面临的棘手难题。探索肺癌全身转移的诱因、机制对于临床上肺癌的治疗及改善患者预后具有重要意义。低氧肿瘤微环境是肿瘤增殖、侵袭、转移的重要调节因素,而肿瘤新血管的生成是其中... 详细信息

研究目的肺癌的恶性转移和复发是临床治疗过程中经常面临的棘手难题。探索肺癌全身转移的诱因、机制对于临床上肺癌的治疗及改善患者预后具有重要意义。低氧肿瘤微环境是肿瘤增殖、侵袭、转移的重要调节因素,而肿瘤新血管的生成是其中的基础。本研究旨在阐明低氧诱导线粒体中akt2-PDK1通路调控YKL-40在肺癌侵袭性生长和血管新生中的作用,为临床上肺癌的治疗提供新的靶点和思路。实验方法1、比较强侵袭性肺癌细胞系CL1-5在常氧和低氧环境培养下,线粒体中akt2和PDK1的富集和磷酸化水平,细胞内HIF-1α,YKL-40,VEGF,TGF-β等蛋白的表达和分泌。2、构建akt2 sh RNA、YKL-40过表达慢病毒载体,转染CL1-5细胞系,比较akt2干扰和/或YKL-40过表达对CL1-5细胞中PDK1磷酸化,YKL-40,VEGF,TGF-β等蛋白的表达和分泌的影响;通过CCK8,Transwell实验和成管能力检测等方法检测细胞活性、迁移、侵袭和血管新生能力。3、将上述处理细胞系分别构建裸鼠皮下荷瘤模型,观察akt2干扰和/或YKL-40过表达的CL1-5细胞的成瘤能力。4、在第32天收集各组肿瘤组织,通过免疫印迹检测小鼠肿瘤中akt2和PDK1的富集和磷酸化水平,YKL-40,VEGF,TGF-β等蛋白的表达,通过免疫组化比较各组肿瘤细胞的增殖活性和血管生成能力。实验结果1、低氧处理CL1-5细胞能明显增加线粒体中akt2、PDK1的磷酸化水平,细胞内p-Smad3、YKL-40和HIF-1α蛋白表达增加,细胞TGF-β、YKL-40、VEGF的分泌增加。2、CL1-5细胞转染akt2 sh RNA载体,并在低氧环境下处理24 h,akt2、p-akt2、YKL-40、p-Smad3、HIF-1α蛋白、N-cadherin和Vimentin表达均明显降低,E-cadherin蛋白表达增加。经过YKL-40过表达载体转染后,细胞YKL-40、N-cadherin、Vimentin蛋白明显增加,而E-cadherin蛋白表达却减少,akt2和p-akt2、p-Smad3、HIF-1α蛋白则无明显改变。收集上清akt2 sh RNA稳转株细胞因子分泌降低,经过YKL-40过表达载体转染后,细胞TGF-β、YKL-40、VEGF分泌增加。3、低氧条件下akt2干扰后,抑制了CL1-5细胞增殖、迁移、侵袭和小管生成;而YLK-40过表达能促进CL1-5细胞增殖、迁移、侵袭和小管生成。4、小鼠皮下注射各组处理的CL1-5细胞,akt2 sh RNA稳转株注射小鼠肿瘤增长速度明显小于对照组,而经过YKL-40过表达病毒感染的akt2 sh RNA稳转株注射小鼠肿瘤体积明显增大。第32天称量小鼠肿瘤,akt2 sh RNA稳转株注射的小鼠肿瘤的重量明显小于对照组,而经过YKL-40过表达病毒感染的akt2 sh RNA稳转株注射的小鼠肿瘤重量明显增加。5、与Scramble组的小鼠相比,akt2 sh RNA组小鼠肿瘤的p-PDK1、HIF-1α、TGF-β、p-Smad3、YKL-40、N-cadherin、vimentin、VEGF蛋白表达均明显减少,而E-cadherin蛋白表达却相应增多。YKL-40过表达病毒感染的肿瘤akt2、p-akt2、p-PDK1、HIF-1α、p-Smad3、PDK1和Smad3蛋白无明显变化,TGF-β、YKL-40、N-cadherin、vimentin、VEGF蛋白表达均明显增多,而E-cadherin蛋白表达则出现减少。akt2 sh RNA小鼠肿瘤Ki67阳性率明显下降,细胞增殖减少,v WF阳性表达明显出现降低,血管新生减少。与空载病毒感染组相比,YKL-40过表达病毒感染后的稳转株注射小鼠,肿瘤Ki67阳性率明显增加,说明细胞增殖增加,v WF阳性表达增加,说明血管新生增加。实验结论本研究发现肺癌细胞在低氧微环境下,通过线粒体中akt2-PDK1聚集和磷酸化上调HIF-1α,YKL-40表达,促进肺癌细胞增殖、侵袭、迁移和血管新生。研究还通过构建干扰RNA和过表达载体,在细胞实验和动物实验水平验证akt2-PDK1-YKL-40通路的存在和促进肺癌恶性表型的作用。

关键词：肺癌 akt2 YKL-40 血管新生

RNA-binding protein LIN28B inhibits apoptosis through regulation of the akt2/FOXO3A/BIM axis in ovarian cancer cells

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Signal Transduction and Targeted Therapy 2018年第1期3卷 96-106页

作者： Xiaojuan Lin Jianfeng Shen Dan Peng Xinhong He Congjian Xu Xiaojun Chen Janos LTanyi Kathleen Montone Yi Fan Qihong Huang Lin Zhang Xiaomin Zhong Center for Research on Reproduction and Women’s Health University of PennsylvaniaPhiladelphiaPA 19104USA Department of Gynecology and Obstetrics Key Laboratory of Obstetrics&Gynecologic and Pediatric Diseases and Birth Defects of Ministry of EducationWest China Second HospitalSichuan UniversityChengdu 610041P.R.China Key Laboratory for Stem Cells and Tissue Engineering Ministry of EducationCenter for Stem Cell Biology and Tissue EngineeringDepartment of BiologyZhongshan School of MedicineSun Yat-Sen UniversityGuangzhou 510080P.R.China Beijing Friendship Hospital Capital Medical UniversityBeijing 100050P.R.China Obstetrics and Gynecology Hospital of Fudan University Shanghai 200011P.R.China Department of Obstetrics and Gynecology University of PennsylvaniaPhiladelphiaPA 19104USA Department of Pathology and Laboratory Medicine University of PennsylvaniaPhiladelphiaPA 19104USA Department of Radiation Oncology University of PennsylvaniaPhiladelphiaPA 19104USA Shanghai Respiratory Research Institute Shanghai 200032P.R.China Department of Pulmonary and Critical Care Medicine Zhongshan HospitalFudan UniversityShanghai 200032P.R.China Institute of Clinical Science Zhongshan HospitalFudan UniversityShanghai 200032P.R.China

LIN28B is an evolutionarily conserved RNA-binding protein that regulates mRNA translation and miRNA let-7 maturation in embryonic stem cells and developing tissues.Increasing evidence demonstrates that LIN28B is activated in cancer and serves as a critical oncogene.However,the underlying molecular mechanisms of LIN28B function in tumorigenesis are still largely unknown.Here we report that LIN28B was expressed in over half of the patients with epithelial ovarian cancer who were examined(n=584).Functional experiments demonstrated that LIN28B inhibited ovarian cancer cell apoptosis.Furthermore,we showed that the proapoptotic factor BIM played an essential role in the antiapoptotic function of LIN28B.RNA-IP microarray analysis suggested that LIN28B binds to mRNAs that are associated with the DNA damage pathway,such as akt2,in ovarian cancer cells.By binding to akt2 mRNA and enhancing its protein expression,LIN28B regulated FOXO3A protein phosphorylation and decreased the transcriptional level of BIM,which antagonized the antiapoptosis activity of LIN28B.Taken together,these results mechanistically linked LIN28B and the akt2/FOXO3A/BIM axis to the apoptosis pathway.The findings may have important implications in the diagnosis and therapeutics of ovarian cancer.

关键词： akt2 diagnosis apoptosis