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smad7 expression in CAR-T cells improves persistence and safety for solid tumors

Cellular & Molecular Immunology 2024年第3期21卷 213-226页

作者： Sixin Liang Rui Zheng Baile Zuo Jia Li Yiyi Wang Yujie Han Hao Dong Xiaojuan Zhao Yiting Zhang Pengju Wang Ruotong Meng Lintao Jia Angang Yang Bo Yan State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers Department of Biochemistry and Molecular BiologyFourth Military Medical UniversityXi’anShaanxi710032China School of Medicine Technology Xinxiang Medical UniversityXinxiangHenan453003China Department of Obstetrics and Gynecology Xijing Hospital of Fourth Military Medical UniversityXi’anShaanxi710032China College of Life Science Yan’an UniversityYan’anShaanxi716000China Department of Immunology Fourth Military Medical UniversityXi’anShaanxi710032China

Despite the tremendous progress of chimeric antigen receptor T(CAR-T)cell therapy in hematological malignancies,their application in solid tumors has been limited largely due to T-cell exhaustion in the tumor microenvironment(TME)and systemic toxicity caused by excessive cytokine release.As a key regulator of the immunosuppressive TME,TGF-βpromotes cytokine synthesis via the NF-κB pathway.Here,we coexpressed smad7,a suppressor of TGF-βsignaling,with a HER2-targeted CAR in engineered T cells.These novel CAR-T cells displayed high cytolytic efficacy and were resistant to TGF-β-triggered exhaustion,which enabled sustained tumoricidal capacity after continuous antigen exposure.Moreover,smad7 substantially reduced the production of inflammatory cytokines by antigen-primed CAR-T cells.Mechanistically,smad7 downregulated TGF-βreceptor I and abrogated the interplay between the TGF-βand NF-κB pathways in CAR-T cells.As a result,these CAR-T cells persistently inhibited tumor growth and promoted the survival of tumor-challenged mice regardless of the hostile tumor microenvironment caused by a high concentration of TGF-β.smad7 coexpression also enhanced CAR-T-cell infiltration and persistent activation in patient-derived tumor organoids.Therefore,our study demonstrated the feasibility of smad7 coexpression as a novel approach to improve the efficacy and safety of CAR-T-cell therapy for solid tumors.

关键词： TGF-βpathway smad7 NF-κB pathway CAR-T-cell therapy Cytokine release syndrome(CRS)

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基于微小RNA21-5p靶向smad7探讨沙库巴曲缬沙坦抗射血分数保留心力衰竭心肌纤维化的机制

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中国医院药学杂志 2024年第8期44卷 882-889页

作者：石玉姣杨晨光乔文博刘永成刘思雨董国菊中国中医科学院西苑医院心血管内科北京100091 中国中医科学院西苑医院/国家中医心血管病临床医学研究中心北京100091

目的:基于微小RNA21-5p(miRNA21)靶向smad7探讨沙库巴曲缬沙坦(LCZ696)抗射血分数保留心力衰竭(HFpEF)心肌纤维化的机制。方法:10只Wistar Kyoto(WKY)大鼠和10只自发性高血压大鼠(SHR)作为对照组。20只SHR大鼠平均分为HFpEF和LCZ696组,... 详细信息

目的:基于微小RNA21-5p(miRNA21)靶向smad7探讨沙库巴曲缬沙坦(LCZ696)抗射血分数保留心力衰竭(HFpEF)心肌纤维化的机制。方法:10只Wistar Kyoto(WKY)大鼠和10只自发性高血压大鼠(SHR)作为对照组。20只SHR大鼠平均分为HFpEF和LCZ696组,给予高脂-盐-糖饮食及腹腔注射链脲霉素建立HFpEF大鼠模型。造模成功后,干预组给予LCZ696(18 mg·kg^(–1)·d^(–1))治疗6周。治疗结束后,行超声心动图测量左心室(LV)舒张末内径(LVEDd)、前壁厚度(LVAWd)、后壁厚度(LVPWd)、射血分数(LVEF)、等容舒张时间(IVRT)、舒张早期二尖瓣流入峰值速度(E)/二尖瓣环运动速度(e');斑点追踪超声心动图测量全纵向应变(GLS)及应变率(GLSr);ELISA法检测血清心房钠尿肽(ANP)、B型利钠肽(BNP)及半乳糖凝集素3(Gal-3);心肌进行Masson染色,观察心肌纤维化情况,并计算胶原体积分数(CVF)及血管周围纤维化比率(PFR);qPCR及Western blot检测LV心肌目的基因及蛋白表达情况。结果:与对照组比较,HFpEF组的LVEDd、LVAWd、LVPWd、IVRT、E/e'、GLS及GLSr的绝对值、ANP、BNP、Gal-3、CVF和PFR显著升高(Psmad2、smad3 mRNA表达和α-SMA、CollⅠ、CollⅢ、P-smad2、P-smad3蛋白表达显著上调(Psmad7 mRNA及蛋白表达显著下调(Psmad2、smad3 mRNA表达和α-SMA、CollⅠ、P-smad2及P-smad3蛋白表达显著下调(Psmad7 mRNA及蛋白表达显著上调(Psmad7表达,从而抗心肌纤维化,进一步改善HFpEF大鼠的LV重塑和功能障碍。

关键词：沙库巴曲缬沙坦钠射血分数保留心力衰竭微小RNA21-5p smad7 心肌纤维化

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心房颤动患者TGF-β1/smad2、smad7信号通路在心房肌重构表达的研究

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现代诊断与治疗 2024年第3期35卷 317-321页

作者：方曙罗怡文杨人强徐杏安南昌县人民医院江西南昌330200 南昌市西湖区朝阳洲街道卫生服务中心江西南昌330000 南昌大学第二附属医院心血管内科江西南昌330006

目的探讨TGF-β1信号通路中的smad2、smad7表达分布变化与房颤纤维化的发生、发展的关系。方法选取2018年1月至2020年12月于我院行心脏外科手术患者52例,按病变性质分为房颤组24例(RAF)和窦律组28例(RSR),通过检测心外科手术患者房颤及... 详细信息

目的探讨TGF-β1信号通路中的smad2、smad7表达分布变化与房颤纤维化的发生、发展的关系。方法选取2018年1月至2020年12月于我院行心脏外科手术患者52例,按病变性质分为房颤组24例(RAF)和窦律组28例(RSR),通过检测心外科手术患者房颤及窦性心律组右心房组织中的smad2、smad7、纤维化因子Fibronectin的表达,比较smad2、smad7表达量、空间分布及Fibronectin表达量变化。结果房颤患者右心房smad2表达量明显高于窦性心律组,而smad7表达量明显低于窦性心律患者,纤维化因子Fibronectin表达量明显高于窦性心律组,差异有统计学意义(Psmad2、smad7信号通路参与房颤心房纤维化所致结构重构。

关键词：心房颤动 smad2 smad7 心房纤维化

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哮喘小鼠肺组织smad2和smad7及转化生长因子-β1蛋白表达与气道重塑的关系

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中华实用诊断与治疗杂志 2024年第4期38卷 336-341页

作者：娄春艳李敏李丽吴星河南省人民医院郑州大学人民医院儿科河南郑州450003 四川省医学科学院四川省人民医院儿科四川成都610072 四川省医学科学院四川省人民医院城东病区儿科四川成都610110

目的观察哮喘小鼠气道重塑过程中肺组织smad2、smad7、转化生长因子-β_(1)(TGF-β_(1))蛋白表达变化,分析其与气道重塑的关系。方法SPF级Balb/c雌性小鼠48只,随机分为模型组、对照组各24只,模型组实验第0、14天腹腔注射含20μg卵清蛋白... 详细信息

目的观察哮喘小鼠气道重塑过程中肺组织smad2、smad7、转化生长因子-β_(1)(TGF-β_(1))蛋白表达变化,分析其与气道重塑的关系。方法SPF级Balb/c雌性小鼠48只,随机分为模型组、对照组各24只,模型组实验第0、14天腹腔注射含20μg卵清蛋白和100μg氢氧化铝的生理盐水混悬液致敏,第21天起给予质量分数2.5%卵清蛋白溶液雾化吸入激发(隔天1次,每次30min)制备哮喘模型,对照组给予等体积生理盐水。分别于激发2、4、8周后的24h内2组各随机处死8只小鼠,取左肺组织及主支气管,采用HE染色行组织病理检查,测定气道形态学参数支气管总管壁面积(WAt)/支气管基底膜周径(Pbm)、支气管内壁面积(WAi)/Pbm、支气管平滑肌面积(WAm)/Pbm;采用免疫组织化学SP法检测肺组织smad2、smad7、TGF-β_(1)蛋白表达,测定光密度值。采用Pearson相关法分析模型组肺组织smad2、smad7、TGF-β_(1)蛋白光密度值与WAt/Pbm、WAm/Pbm的相关性。结果(1)模型组激发2、4、8周时可见支气管壁及血管周围有大量炎症细胞浸润,部分细支气管上皮细胞脱落不全,杯状细胞增生伴黏液大量分泌,气道平滑肌细胞增生,基底膜增厚;随激发时间延长,气道平滑肌细胞增生及基底膜增厚越明显。(2)模型组激发2、4、8周时WAt/Pbm[(71.8±15.2)、(68.8±10.2)、(101.1±6.9)μm^(2)/μm]均大于对照组[(44.9±6.1)、(39.9±4.1)、(45.7±8.3)μm^(2)/μm](P0.05);模型组激发4、8周时WAm/Pbm[(8.2±1.4)、(10.9±2.9)μm^(2)/μm]均大于对照组[(6.2±1.0)、(6.0±1.4)μm^(2)/μm](t=3.291,P=0.005;t=4.302,P=0.001),2周时[(7.2±1.1)μm^(2)/μm]与对照组[(6.6±0.6)μm^(2)/μm]比较差异无统计学意义(P>0.05)。激发8周时模型组WAt/Pbm、WAm/Pbm均大于2、4周时(P0.05);激发2、4、8周时模型组WAi/Pbm比较差异无统计学意义(P>0.05)。激发2、4、8周时对照组WAt/Pbm、WAi/Pbm、WAm/Pbm比较差异均无统计学意义(P>0.05)。(3)模型组激发2、4、8周时肺组织smad2蛋白光密度值(0.24±0.01、0.25±0.01、0.26±0.01)均高于对照组(0.21±0.01、0.21±0.02、0.20±0.01)(Psmad7蛋白光密度值(0.19±0.01、0.17±0.01、0.15±0.01)均低于对照组(0.28±0.06、0.29±0.04、0.29±0.02)(P7±0.01、0.16±0.01)均高于对照组(0.14±0.01、0.14±0.01)(P0.05)。激发8周时模型组肺组织smad2蛋白光密度值均高于2、4周时(P0.05);激发2、4、8周时模型组肺组织smad7蛋白光密度值依次降低(P0.05)。激发2、4、8周时对照组肺组织smad2、smad7、TGF-β_(1)蛋白光密度值比较差异均无统计学意义(P>0.05)。(4)激发2、4、8周时模型组肺组织smad2、TGF-β_(1)蛋白光密度值与WAt/Pbm、WAm/Pbm均呈正相关(Psmad7蛋白光密度值与WAt/Pbm、WAm/Pbm均呈负相关(Psmad2、TGF-β_(1)表达升高及smad7表达降低参与哮喘小鼠气道重塑的发生;随激发时间延长,smad2、smad7表达呈动态变化,TGF-β_(1)表达变化不明显。

关键词：哮喘气道重塑 smad2 smad7 转化生长因子-β_(1) 小鼠

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miR‑423 sponged by lncRNA NORHA inhibits granulosa cell apoptosis

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Journal of Animal Science and Biotechnology 2024年第2期15卷 632-644页

作者： Yuqi Li Zhuofan Zhang Siqi Wang Xing Du Qifa Li College of Animal Science and Technology Nanjing Agricultural UniversityNanjing 210095China

Background Atresia and degeneration,a follicular developmental fate that reduces female fertility and is triggered by granulosa cell(GC)apoptosis,have been induced by dozens of miRNAs.Here,we report a miRNA,miR-423,that inhibits the initiation of follicular atresia(FA),and early apoptosis of GCs.Results We showed that miR-423 was down-regulated during sow FA,and its levels in follicles were negatively correlated with the GC density and the P4/E2 ratio in the follicular fluid in vivo.The in vitro gain-of-function experiments revealed that miR-423 suppresses cell apoptosis,especially early apoptosis in GCs.Mechanically speaking,the miR-423 targets and interacts with the 3’-UTR of the porcine smad7 gene,which encodes an apoptosis-inducing factor in GCs,and represses its expression and pro-apoptotic function.Interestingly,FA and the GC apoptosis-related lncRNA NORHA was demonstrated as a ceRNA of miR-423.Additionally,we showed that a single base deletion/insertion in the miR-423 promoter is significantly associated with the number of stillbirths(NSB)trait of sows.Conclusion These results demonstrate that miR-423 is a small molecule for inhibiting FA initiation and GC early apoptosis,suggesting that treating with miR-423 may be a novel approach for inhibiting FA initiation and improving female fertility.

关键词： Granulosa cell apoptosis miR-423 NORHA smad7 Sow fertility traits

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Corrigendum to “Sox9 augments BMP2-induced chondrogenic differentiation by downregulating smad7 in mesenchymal stem cells (MSCs)” [Genes & Diseases 4 (2017) 229–239]

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Genes & Diseases 2023年第2期10卷 624-626页

作者： Chen Zhao Wei Jiang Nian Zhou Junyi Liao Mingming Yang Ning Hu Xi Liang Wei Xu Hong Chen Wei Liu Lewis L. Shi Leonardo Oliveira Jennifer Moriatis Wolf Sherwin Ho Aravind Athiviraham H.M. Tsai Tong-Chuan He Wei Huang Department of Orthopedic Surgery The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Molecular Oncology Laboratory Department of Orthopaedic Surgery and Rehabilitation MedicineThe University of Chicago Medical CenterChicagoIL 60637USA Department of Radiology The University of ChicagoChicagoIL 60637USA

The authors regret having image assembly errors in Figure 1A and Figure 3A.Specifically,in Figure 1A,the images for"C3H10T1/2",""BMP2"and"Sox9"were erroneously duplicated with the images from an irrelevant experiment that was conducted at the same time.In Figure 3A,the images for"Col2a1"and"β-actin"were erroneously duplicated with the images from an irrelevant experiment that was conducted at the same time.

关键词： smad7 Figure BMP2

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Expression of smad7 inhibits fibrogenic responses of keratocytes to transforming growth factor β2

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Chinese Medical Journal 2011年第13期124卷 1988-1993页

作者： WANG Ti ZHOU Xing-tao YU Yan DAI Jin-hui QU Xiao-mei LE Qi-hua CHU Ren-yuan Department of Ophthalmology Eye & ENT Hospital of FudanUniversity Shanghai 200031 China Department of Safety Assessment Merck Research Laboratories West Point Pennsylvania USA

Background Transforming growth factor β （TGFβ） is one of the most important growth factors in the development of fibrosis and scarring on cornea. smad7, an inhibitory smad, can inhibit TGFβ signal transduction. In recent years, effects of lentiviral-mediated smad7 on inhibition of fibrosis on some organs have been studied, while little is known about the effects on cornea. This study aimed to determine the effects of lentiviral-mediated smadTgene expression on keratocyte proliferation and fibrosis induced by TGF β2 in vitro. Methods Keratocytes were cultured from corneal tissue isolated from Sprague-Dawley （SD） rats and transfected with smad7 expressing lentiviral vector （Lv-smad7） or non-functioning control vector （Lv-blank）. Following the exposure to TGFβ2, keratocytes were processed for immunoblotting to assess the phosphorylation of smad2 as down-stream event of TGFβ/smad signaling. Expression of fibrotic markers a-smooth muscle actin （a-SMA）, type III collagen （collagen III） were measured by Western blotting and quantitative real time polymerase chain reaction （PCR）. Overall cell proliferation was determined by 3-（4,5-dimethyl-thiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and the expression of cell cycle-related marker Ki67 at both mRNA and protein levels. Results The smad7 gene transfer suppressed TGFβ/smad signaling in keratocytes by down-regulating phosphorylation of smad2. Markers of cell proliferation and fibrosis including Ki67, a-SMA, collagen III were inhibited by introduction of smad 7 into TGFβ exposed keratocytes. Consequently, the rate of cell proliferation was attenuated. Conclusion smad7gene transfer inhibited fibrogenic responses of keratocytes to TGFβ2.

关键词： cornea proliferation fibrosis smad7 transforming growth factorf β

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smad7 dependent expression signature highlights BMP2 and HK2 signaling in HSC transdifferentiation

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World Journal of Gastroenterology 2010年第41期16卷 5211-5224页

作者： Bernd Denecke Lucia Wickert Loredana Ciuclan Steven Dooley Nadja M Meindl-Beinker Yan Liu Interdisciplinary Centre for Clinical Research (IZKF) Aachen RWTH Aachen University 52074 Aachen Germany Institute of Clinical Chemistry and Pathobiochemistry of RWTH-University Hospital Department of Biology Babes-Bolyai University 400084 Cluj-Napoca Romania Molecular Hepatology Alcohol Induced Diseases Department of Medicine Ⅱ Medical Faculty Mannheim University of Heidelberg 68167 Mannheim

AIM: To analyse the influence of smad7, antagonist of transforming growth factor (TGF)-β canonical signaling pathways on hepatic stellate cell (HSC) transdifferentia-tion in detail. METHODS: We systematically analysed genes regulated by TGF-β/smad7 in activated HSCs by microarray analy-sis and validated the results using real time polymerase chain reaction and Western blotting analysis. RESULTS: We identif ied 100 known and unknown tar-gets underlying the regulation of smad7 expression and delineated 8 gene ontology groups. Hk2, involved in glycolysis, was one of the most downregulated proteins, while BMP2, activator of the smad1/5/8 pathway, was extremely upregulated by smad7. However, BMP2 de-pendent smad1 activation could be inhibited in vitro by smad7 overexpression in HSCs. CONCLUSION: We conclude (1) the existence of a tight crosstalk of TGF-β and BMP2 pathways in HSCs and (2) a smad7 dependently decreased sugar metabolism ameliorates HSC activation probably by energy with-drawal.

关键词： Transforming growth factor-β smad7 Hepatic stellate cell Gene regulation Glucose metabolism BMP2

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Role of smad7 in inflammatory bowel diseases

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World Journal of Gastroenterology 2012年第40期18卷 5664-5668页

作者： Giovanni Monteleone Roberta Caruso Francesco Pallone Department of Internal Medicine University Tor Vergata of Rome

Crohn's disease and ulcerative colitis,the major forms of inflammatory bowel diseases(IBD) in man,are complex diseases in which genetic and environmental factors interact to promote an excessive mucosal immune response directed against normal components of the bacterial microflora.There is also evidence that the pathologic process is due to defects in counterregulatory mechanisms,such as those involving the immunosuppressive cytokine transforming growth factor(TGF)-1.Indeed,studies in human IBD tissues and murine models of colitis have documented a disruption of TGF-1 signalling marked by a block in the phosphorylation of smad3,a signalling molecule associated with the activated TGF-receptor,due to up-regulation of smad7,an intracellular inhibitor of smad3 phosphorylation.Knock-down of smad7 with a specific antisense oligonucleotide restores TGF-1/smad3 signalling,thus resulting in a marked suppression of inflammatory cytokine production and attenuation of murine colitis.These findings together with the demonstration that smad7 antisense oligonucleotide is not toxic when administered in mice have paved the way for the development of a smad7 antisense oligonucleotidebased pharmaceutical compound that is now ready to enter the clinics.In this article we review the available data supporting the pathogenic role of smad7 in IBD and discuss whether and how smad7 antisense therapy could help dampen the ongoing inflammation in IBD.

关键词： smad7 肠道疾病炎症溃疡性结肠炎反义寡核苷酸炎性细胞因子 smad3 TGF-β

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smad7介导TGF-β信号通路对绵羊卵泡颗粒细胞增殖的影响

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中国农业科学 2023年第13期56卷 2597-2608页

作者：郭泽媛杜张胜张雅琦陈春路马晓燕成颖王锴吕丽华山西农业大学动物科学学院

【目的】卵泡发育是一个复杂的调控过程，其中绵羊卵泡颗粒细胞（granulosa cells, GCs）的增殖，分化会直接影响卵泡的发育状况。TGF-β信号通路在绵羊卵巢发育和卵泡生长过程中起着重要作用，smad7作为TGF-β信号通路关键性的抑制基... 详细信息

【目的】卵泡发育是一个复杂的调控过程，其中绵羊卵泡颗粒细胞（granulosa cells, GCs）的增殖，分化会直接影响卵泡的发育状况。TGF-β信号通路在绵羊卵巢发育和卵泡生长过程中起着重要作用，smad7作为TGF-β信号通路关键性的抑制基因也发挥重要作用，通过探究smad7介导TGF-β信号通路对绵羊卵泡GCs增殖凋亡的影响，为进一步研究smad7在卵泡GCs增殖凋亡过程中的调控作用提供依据。【方法】选取4—6月龄未怀孕的晋中健康杜湖杂交母羊20只，屠宰后采集双侧卵巢组织，分离培养卵泡颗粒细胞，FSHR细胞免疫荧光鉴定，smad7细胞免疫荧光的表达定位，CCK8法测定细胞增殖情况，绘制生长曲线；细胞传代后外源添加不同浓度smad7激动剂积雪草苷（asiaticoside,AS）(0、100、200、400、600 ng·mL-1)培养绵羊卵泡GCs，选择AS最佳作用浓度处理二代颗粒细胞，采用实时荧光定量PCR和Western blotting检测TGF-β信号通路中关键基因及细胞凋亡和周期相关基因表达水平；合成3个sismad7，转染至卵泡GCs中，选择干扰效果最佳的，采用实时荧光定量PCR和Western blotting检测TGF-β信号通路中关键基因及细胞凋亡和周期相关基因表达水平。【结果】smad7在绵羊卵泡GCs中有表达；200 ng·mL-1 AS能极显著上调smad7在GCs的表达（P smad7-1对绵羊卵泡GCs的转染效果最佳（Psmad7上调能显著增加TGF-β信号通路smad4,TFDP-1和EP300的表达量（P7的表达量（Psmad7 siRNA显著降低TGF-β信号通路smad4,TFDP-1和EP300的表达量（P7和CCND2的表达量（Psmad7上调，GCs的增殖率在24和48 h显著下调（Psmad7 siRNA在24和72 h显著升高GCs的增殖率（Psmad7介导TGF-β信号通路抑制绵羊卵泡GCs增殖和促进细胞凋亡。

关键词：积雪草苷 siRNA smad7 TGF-β信号通路绵羊颗粒细胞

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