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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 *** a key regulator of the immunosuppressive TME,TGF-βpromotes cytokine synthesis via the NF-κB ***,we coexpressed smad7,a suppressor of TGF-βsignaling,with a HER2-targeted CAR in engineered T *** novel CAR-T cells displayed high cytolytic efficacy and were resistant to TGF-β-triggered exhaustion,which enabled sustained tumoricidal capacity after continuous antigen ***,smad7 substantially reduced the production of inflammatory cytokines by antigen-primed CAR-T ***,smad7 downregulated TGF-βreceptor I and abrogated the interplay between the TGF-βand NF-κB pathways in CAR-T *** 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 ***,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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外泌体源性miRNA-21-5p/smad7在石英粉尘致大鼠肺纤维化中的作用

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环境与职业医学 2024年第8期41卷 861-866页

作者：卢炀丁晓慧王甜甜徐萌彤郝嘉瑞李文静宋静山西医科大学公共卫生学院山西医科大学煤炭环境致病与防治教育部重点实验室山西医科大学国家卫健委尘肺病重点实验室

[背景]石英粉尘在肺部无法降解，职业生产过程中吸入大量石英粉尘会导致肺纤维化的发生，进而发展为矽肺病。近年来，研究发现外泌体可能通过携带微小核糖核酸（miRNA）参与纤维化疾病的发病过程，但其在矽肺进程中的作用机制仍然有待... 详细信息

[背景]石英粉尘在肺部无法降解，职业生产过程中吸入大量石英粉尘会导致肺纤维化的发生，进而发展为矽肺病。近年来，研究发现外泌体可能通过携带微小核糖核酸（miRNA）参与纤维化疾病的发病过程，但其在矽肺进程中的作用机制仍然有待研究。[目的]研究外泌体源miRNA-21-5p/抗生物皮肤生长因子母体同源蛋白7（smad7）在石英粉尘致大鼠肺纤维化的中作用。[方法] 24只健康雄性SD大鼠被随机分为4组（每组6只）：对照4周组、对照16周组和石英4周组、石英16周组。在实验开始时，采用一次性非暴露式气管内染尘的方式分别向石英组和对照组大鼠气管内注入1 mL石英悬液(50 mg·mL-1)和1 mL生理盐水。染尘后第4周、16周行肺泡灌洗术获取肺泡灌洗液，采用聚乙二醇（PEG）沉淀法提取灌洗液内的外泌体，透射电子显微镜（TEM）进行形态学的鉴定，纳米追踪分析（NTA）检测外泌体的粒径，免疫印迹法（WB）检测外泌体的标志蛋白CD9和CD63。采用逆转录聚合酶链反应（RT-PCR）法测定外泌体内miRNA-21-5p的表达水平；采用苏木精-伊红染色法（HE）染色及马松染色法（Masson）观察大鼠肺组织损伤及纤维化病变程度；采用羟脯氨酸（HYP）法检测肺组织胶原含量；采用WB检测肺组织smad7蛋白的表达。[结果]病理染色结果显示，与对照组相比，染尘4周后大鼠肺组织炎细胞浸润，肺泡壁增厚，胶原蛋白增多，染尘16周后出现胶原蛋白沉积和矽结节；与对照组相比，染尘4周、16周时石英组大鼠肺组织中HYP的表达水平均增高（P smad7蛋白表达量均降低（P smad7可能参与了石英粉尘致大鼠肺纤维化的作用机制。

关键词：石英粉尘外泌体 miRNA-21-5p smad7 肺纤维化

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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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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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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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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 *** 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)-***,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 ***-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 *** 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 *** 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： Inflammatory bowel diseases Gut inflam-mation Transforming growth factor-β1 smad7 Anti-sense oligonucleotides

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miR-34c inhibits proliferation and enhances apoptosis in immature porcine Sertoli cells by targeting the smad7 gene

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Journal of Integrative Agriculture 2019年第2期18卷 449-459页

作者： RAN Mao-liang WENG Bo CAO Rong PENG Fu-zhi LUO Hui GAO Hu CHEN Bin College of Animal Science and Technology/Hunan Provincial Key Laboratory for Genetic Improvement of Domestic Animal Hunan Agricultural UniversityChangsha 410128P.R.China

MicroRNAs(miRNAs) are implicated in swine spermatogenesis via their regulations of cell proliferation, apoptosis, and differentiation. Recent studies indicated that miR-34 c is indispensable in the late steps of spermatogenesis. However, whether miR-34 c plays similar important roles in immature porcine Sertoli cells remain unknown. In the present study, we conducted two experiments using a completely randomised design to study the function roles of miR-34 c. The results from experiment I demonstrated that the relative expression level of miR-34 c in swine testicular tissues increased(P=0.0017) quadratically with increasing age, while the relative expression level of smad family member 7(smad7) decreased(P=0.0009) with curve. Furthermore, miR-34 c expression levels showed a significant negative correlation(P=0.013) with smad7 gene expression levels. The results from experiment II indicated that miR-34 c directly targets the smad7 gene using a luciferase reporter assay, and suppresses(Psmad7 mRNA and protein expressions in immature porcine Sertoli cells. Overexpression of miR-34 c inhibited(Psmad7 via small interfering RNA(siR NA) gave a similar result. It is concluded that miR-34 c inhibits proliferation and enhances apoptosis in immature porcine Sertoli cells by targeting the smad7 gene.

关键词： immature porcine Sertoli cell cell proliferation apoptosis smad7 miR-34c

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Roles of smad3 and smad7 in rat pancreatic stellate cells activated by transforming growth factor-beta 1

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Hepatobiliary & Pancreatic Diseases International 2010年第5期9卷 531-536页

作者： Qian, Zhu-Yin Peng, Quan Zhang, Zheng-Wei Thou, Long-An Miao, Yi Nanjing Med Univ Affiliated Hosp 1 Dept Gen Surg Nanjing 210029 Peoples R China

BACKGROUND: Pancreatic stellate cells (PSCs) play a major role in promoting pancreatic fibrosis. Transforming growth factor beta 1 (TGF-beta 1) is a critical mediator of this process. This study aimed to determine the expression of the smad3 and smad7 genes in the process of PSC activation, and explore the mechanisms of chronic pancreatitis. METHODS: The expressions of smad3 and smad7 in PSCs before and after TGF-beta 1 treatment were detected by reverse transcription-polymerase chain reaction and Western blotting analysis. smad3 expression was detected in PSCs after treatment with 5 ng/ml of TGF-beta 1 for 24 hours. RESULTS: smad7 expression was decreased in TGF-beta 1 -activated PSCs (Psmad3, smad3, and smad7 was inhibited (Psmad3 and inhibits the expression of smad7 during the activation of PSCs. In contrast, high-dose TGF-beta 1 downregulates the expression of smad3 in completely activated PSCs.

关键词： pancreatic stellate cell transforming growth factor beta 1 chronic pancreatitis smad3 smad7

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The role of smad7 in oral mucositis

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Protein & Cell 2015年第3期6卷 160-169页

作者： Li Bian Gangwen Han Carolyn W. Zhao Pamela J. Garl Xiao-Jing Wang Department of Pathology The First Affiliated Hospital of Kunming Medical University Kunming 650032 China Department of Pathology University of Colorado Anschutz. Medical Campus Aurora CO 80203 USA Department of Dermatology The Second Hospital of Shandong University Jinan 250033 China

Oral mucositis, a severe oral ulceration, is a common toxic effect of radioor chemoradio-therapy and a limiting factor to using the maximum dose of radiation for effective cancer treatment. Among cancer patients, at least 40% and up to 70%, of individuals treated with standard chemotherapy regimens or upper-body radiation, develop oral mucositis. To date, there is no FDA approved drug to treat oral mucositis in cancer patients. The key challenges for oral mucositis treatment are to repair and protect ulcerated oral mucosa without promoting cancer cell growth. Oral mucositis is the result of complex, multifaceted pathobiology, involving a series of signaling pathways and a chain of interactions between the epithelium and submucosa. Among those pathways and interactions, the activation of nuclear factor-kappa B （NF-KB） is critical to the inflamma- tion process of oral mucositis. We recently found that activation of TGFβ （transforming growth factor β） signaling is associated with the development of oral mucositis. smad7, the negative regulator of TGFβ signaling, inhibits both NF-KB and TGFβ activation and thus plays a pivotal role in the prevention and treatment of oral mucositis by attenuating growth inhibition, apoptosis, and inflammation while promoting epithelial migration. The major objective of this review is to evaluate the known functions of smad7, with a particular focus on its molecular mechanisms and its function in blocking multiple pathological processes in oral mucositis.

关键词： smad7 oral mucositis cancer TGFβ,NF-κB

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