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Effect of TGF-β/smad signaling pathway on lung myofibroblast differentiation

Acta Pharmacologica Sinica 2007年第3期28卷 382-391页

作者： Li GU~2 Yuan-jue ZHU~(2,4) Xiao YANG~3 Zi-Jian GUO~2 Wen-bing XU~2 Xin-lun TIAN~22 Department of Pulmonary Medicine,Peking Union Medical College Hospital,Chinese Academy of Medical Sciences,Beijing 100071 China 3 Genetic Laboratory of Development and Diseases,Institute of Biotechnology,Beijing 100070,China Department of Pulmonary Medicine Peking Union Medical College Hospital Chinese Academy of Medical Sciences Beijing China Department of Genetic Laboratory of Development and Diseases Institute of Biotechnology Beijing China

Aim:Myofibroblasts play important roles in the pathogenesis of lung fibrosis.Transforming growth factor（TGF）-β1has been widely recognized as a keyfibrogenic cytokine.The major signaling pathway of TGF--β1is through cytoplas-mic smad proteins.Our study investigated the role of individual TGF--β1/smadsignal proteins in mediating α-smooth muscle actin（α-SMA）gene expression,which is a well-known key marker of myofibroblast differentiation.Methods:Wetransiently cotransfected α-SMA promoter-luciferase fusion plasmid（p895-Luc）and smad expression plasmids and measured Luc activity in TGF--β1-treated hu-man fetal lung fibroblasts.We induced smad3 knockout mice lung fibrosis bybleomycin,α-SMA protein expression was assessed by Western blotting.Col-lagen protein was analyzed by measuring hydroxyprolin.Myofibroblast morphol-ogy was assessed by immunohistochemistry.Results:We found that theoverexpression of smad3,not smad2 markedly increased TGF--β1-induced α-SMApromoter activity and α-SMA protein expression in vitro,whereas the over-expression of dominant negative mutant smad3 and smad7 repressed TGF--β1-induced α-SMA gene expression.Compared to wild-type mice,smad3 knockoutmice showed attenuated lung fibrosis after bleomycin treatment,manifested bylower collagen production and myofibroblast differentiation.Conclusion:Ourstudy suggested TGF--β1/smad3 is a major pathway which regulated themyofibroblast differentiation.This result indicates a potential significance forfuture attempts of attenuating the progression of human lung fibrosis by theinhibition of the smad3 cascade.

关键词： myofibroblasts transforming growth factorβ1 smad

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Identification of a TGF-β/smad/lnc-UTGF positive feedback loop and its role in hepatoma metastasis

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Signal Transduction and Targeted Therapy 2021年第12期6卷 3709-3722页

作者： Meng-Zhi Wu Yi-chuan Yuan Bi-Yu Huang Jin-Xi Chen Bin-Kui Li Jian-Hong Fang Shi-Mei Zhuang MOE Key Laboratory of Gene Function and Regulation School of Life SciencesCollaborative Innovation Center for Cancer MedicineSun Yat-sen UniversityXin Gang Xi Road 135#Guangzhou 510275P.R.China Department of Hepatobiliary Surgery Sun Yat-sen University Cancer CenterDong Feng Road East 651#Guangzhou 510060P.R.China

Aberrant activation of the TGF-β/smad signaling pathway is often observed in hepatocellular carcinoma(HCC).Whether lncRNA regulates the TGF-β/smad signaling remains largely unknown.Here,we identified an oncogenic lncRNA that was upregulated in HCC and was transcriptionally induced by TGF-β(named lnc-UTGF,lncRNA upregulated by TGF-β).Upon TGF-βstimulation,smad2/3 bound to the lnc-UTGF promoter and activated lnc-UTGF expression.In turn,the TGF-β/smad signaling was augmented by overexpressing lnc-UTGF,but was inhibited by silencing lnc-UTGF.Mechanism investigations revealed that lnc-UTGF interacted with the mRNAs of smad2 and smad4 via complementary base-pairing,resulting in enhanced stability of smad2/4 mRNAs.These data suggest a novel TGF-β/smad/lnc-UTGF positive feedback circuitry.Subsequent gain-and loss-of-function analyses disclosed that lnc-UTGF promoted the migration and invasion of hepatoma cells,and this effect of lnc-UTGF was attenuated by repressing smad2/4 expression or by mutating the smad2/4-binding sites in lnc-UTGF.Studies using mouse models further confirmed that in vivo metastasis of hepatoma xenografts was inhibited by silencing lnc-UTGF,but was enhanced by ectopic expression of lncUTGF.The lnc-UTGF level was positively correlated with the smad2/4 levels in xenografts.Consistently,we detected an association of lnc-UTGF upregulation with increase of smad2,smad4,and their metastasis effector SNAIL1 in human HCC.And high lnc-UTGF level was also significantly associated with enhanced metastasis potential,advanced TNM stages,and worse recurrence-free survival.Conclusion:there exists a lnc-UTGF-mediated positive feedback loop of the TGF-βsignaling and its deregulation promotes hepatoma metastasis.These findings may provide a new therapeutic target for HCC metastasis.

关键词： metastasis smad inhibited

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Involvement of Rho-associated coiled-coil kinase signaling inhibition in TGF-β1/smad2,3 signal transduction in vitro

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International Journal of Ophthalmology(English edition) 2017年第12期10卷 1805-1811页

作者： Zhao-Hui Feng Xiao-Hui Zhang Jia-Qi Zhao Jun-Ze Ma Department of Ophthalmology the Second Affiliated Hospital of Xi’an Jiaotong University Medical CollegeXi’an 710004Shaanxi ProvinceChina

AIM：To research the effect of Y-27632,a selective Rhoassociated coiled-coil kinase（ROCK） inhibitor,on TGF-β1/smad2,3 signal transduction in ocular Tenon＇s capsule fi broblasts（OTFs）.METHODS：Primary ocular Tenon＇s capsule fibroblasts had been cultured in vitro.The effect of Y27632 on proliferation of OTF stimulated by lysophosphatidic acid（LPA） was evaluated by MTT colorimetric assay so as to sift out the proper concentrations range of Y-27632 for the next experiment.Real time-polymerase chain reactor（RT-PCR） was to analyze the changes of smad2 and smad3 genes of cells affected by Y-27632,though unaffected by transforming growth factorbeta1（TGF-β1）.Proteins of smad2,smad3,phosphorylated smad2（Ser245/250/255）,and phosphorylated smad3（Ser423/425/203） were respectively quantifi ed by Western blot after OTFs were successively incubated by TGF-β1 and Y-27632.Meanwhile,α-smooth muscular actin（α-SMA） protein was also quantified after the small intervening gene fragments of human smad2 and smad3 were designed,synthesized,and then transfected to OTFs.RESULTS：Y-27632 signifi cantly inhibited OTFs proliferation stimulated by LPA.Also Y-27632 signifi cantly suppressed the expressions of smad2 m RNA,smad2,3 proteins expressions,smad3 phosphorylation at the carboxylic terminals of Ser423/425/203 which had been radically promoted by TGF-β1.Si RNA-smad2,3 suppressed α-SMA expressions,but less effectively than Y-27632.CONCLUSION：The inhibition of ROCK signaling may be a potential therapeutic candidate for the treatment of the fi ltration channel fi brosis.

关键词： ROCK Y-27632 transforming growth factor-betal smad human ocular Tenon＇s capsule fibroblasts

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Amphibian-derived peptide homodimer OA-GL17d promotes skin wound regeneration through the miR-663a/TGF-β1/smad axis

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Burns & Trauma 2022年第1期10卷 416-431页

作者： Yue Zhang Ying Wang Lin Zeng Yixiang Liu Huiling Sun Shanshan Li Siyu Wang Longjun Shu Naixin Liu Saige Yin Junsong Wang Dan Ni Yutong Wu Ying Yang Li He Buliang Meng Xinwang Yang Department of Anatomy and Histology&Embryology Faculty of Basic Medical ScienceKunming Medical UniversityKunming 650500YunnanChina Key Laboratory of Chemistry in Ethnic Medicinal Resources&Key Laboratory of Natural Products Synthetic Biology of Ethnic Medicinal Endophytes State Ethnic Affairs Commission&Ministry of EducationSchool of Ethnomedicine and EthnopharmacyYunnan MinZu UniversityKunming 650504YunnanChina Endocrinology Department of Affiliated Hospital of Yunnan University Kunming 650021YunnanChina Institutional Center for Shared Technologies and Facilities of Kunming Institute of Zoology Chinese Academy of SciencesKunming 650223YunnanChina Department of Dermatology First Affiliated Hospital of Kunming Medical UniversityKunming650500YunnanChina

Background:Amphibian-derived peptides exhibit considerable potential in the discovery and development of new therapeutic interventions for clinically challenging chronic skin wounds.MicroRNAs(miRNAs)are also considered promising targets for the development of effective therapies against skin wounds.However,further research in this field is anticipated.This study aims to identify and provide a new peptide drug candidate,as well as to explore the underlying miRNA mechanisms and possible miRNA drug target for skin wound healing.Methods:A combination of Edman degradation,mass spectrometry and cDNA cloning were adopted to determine the amino acid sequence of a peptide thatwas fractionated from the secretion of Odorrana andersonii frog skin using gel-filtration and reversed-phase high-performance liquid chromatography.The toxicity of the peptide was evaluated by Calcein-AM/propidium iodide(PI)double staining against human keratinocytes(HaCaT cells),hemolytic activity against mice blood cells and acute toxicity against mice.The stability of the peptide in plasma was also evaluated.The prohealing potency of the peptide was determined by MTS,scratch healing and a Transwell experiment against HaCaT cells,full-thickness injury wounds and scald wounds in the dorsal skin of mice.miRNA transcriptome sequencing analysis,enzyme-linked immunosorbent assay,real-time polymerase chain reaction and western blotting were performed to explore the molecular mechanisms.Results:A novel peptide homodimer(named OA-GL17d)that contains a disulfide bond between the 16th cysteine residue of the peptide monomer and the sequence‘GLFKWHPRCGEEQSMWT’was identified.Analysis showed that OA-GL17d exhibited no hemolytic activity or acute toxicity,but effectively promoted keratinocyte proliferation and migration and strongly stimulated the repair of full-thickness injury wounds and scald wounds in the dorsal skin of mice.Mechanistically,OA-GL17d decreased the level of miR-663a to increase the level of transforming growth factor-β1(TGF-β1)and activate the

关键词： MicroRNA miR-663a Wound healing Peptide Amphibian Human keratinocytes OA-G17d Chronic wound Skin Transforming growth factor-β1 smad

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Effects of angiotensin converting enzyme inhibitor,angio-tensin II type I receptor blocker and their combination on postinfarcted ventricular remodeling in rats

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Chinese Medical Journal 2006年第8期119卷 649-655页

作者： ZHANG Rui-ying WANG Lan-feng ZHANG Lei MENG Xiang-ning LI Shao-jun WANG Wu-ru Department of Cardiology First Clinical Hospital Harbin Medical University Harbin 150001 China Department of Pathology First Clinical Hospital Harbin Medical University Harbin 150001 China

Background Transforming growth factor （TGF） β1-smads signal plays an important role in cardiac remodeling following myocardial infarction （MI）. In addition, both angiotensin converting enzyme inhibitor （ACEI） and angiotensin Ⅱ type Ⅰ receptor blocker （ARB） can effectively prevent left ventricular remodeling. The current study focused on whether the combination of ACEI and ARB is more beneficial for preventing ventricular remodeling and whether smad proteins mediate this beneficial effect. Methods MI was induced by ligating the left anterior descending coronary artery in rats. Twenty-four hours after ligation, the survived rats were randomly divided into five groups and treated for 8 weeks： placebo group, ACEI group （benazepril 10 mg · kg^-1· d^-1）, ARB group （irbesartan 50mg · kg^-1· d^-1）, ACEI＋ARB group （benazepril 10 mg · kg^-1· d^-1＋irbesartan 50 mg · kg^-1· d^-1） and control group （sham-operated rats）. After 8 weeks, we examined the following indexes： the ratio of ventricular weight to body weight （VW/BW）, left ventricular end diastolic dimension （LVDd）, ejection fraction （EF）, fractional shortening （FS）, ratio of E-wave to A-wave velocity, collagen of noninfarcted zone, the mRNA expression of TGFβ1, smad 2, and smad 3 by RT-PCR in noninfarcted zone, the protein expression of smad 2 and smad 3 in noninfarcted zone by Western blot. Results VW/BW significantly increased in the placebo groups compared with that in the control group （P〈0.01）. This increase was limited in ACEI, ARB, and combined groups （P〈0.01 compared with placebo group）. There was no significant difference among the three actively treated groups. Collagen was increased in placebo group （5.68±0.5）% compared with that in control group （P〈0.01）. ACEI, ARB and combined treatment attenuated this increase of collagen [（4.3 ± 0.5）%, （3.5 ± 0.5）%, （3.2± 0.4）%] in comparison with that in placebo group （P〈0.01 respectively）. Combined treatment showed more significant effect on collagen deposition. EF and FS significantly decreased, LVDd and E/A signi

关键词： smad ventricular remodeling angiotensin converting enzyme inhibitor angiotensin II type I receptor blocker

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Paclitaxel ameliorates fibrosis in hepatic stellate cells via inhibition of TGF-β/smad activity

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World Journal of Gastroenterology 2010年第26期16卷 3330-3334页

作者： Jun Zhou, De-Wu Zhong, Qun-Wei Wang, Xiong-Ying Miao, Xun-Di Xu, Department of Hepatobiliary Surgery, Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China Department of Hepatobiliary Surgery Second Xiangya Hospital Central South University Changsha 410011 Hunan Province China.

AIM: To investigated if paclitaxel can attenuate hepatic fi brosis in rat hepatic stellate cells (RHSCs). METHODS: RHSCs were cultured in vitro and randomly assigned to four groups: normal control group (treated only with Dulbecco's Modified Eagle's Medium), Taxol group (200 nmol/L paclitaxel was added to the cell culture), transforming growth factor (TGF)-β group (5 ng/mL recombinant human TGF-β1 was added to the cell culture), and TGF-β + Taxol group. TGF-β signaling cascade and status of various extracellular matrix proteins were evaluated by real time reverse transcriptase polymerase chain reaction and Western blotting. RESULTS: The paclitaxel treatment markedly suppressed smad2/3 phosphorylation. This was associated with attenuated expression of collagen Ⅰ and Ⅲ and fi bronectin in RHSCs.CONCLUSION: These data indicate that 200 nmol/L paclitaxel ameliorates hepatic fi brosis via modulating TGF-β signaling, and that paclitaxel may have some therapeutic value in humans with hepatic fi brosis.

关键词： Transforming growth factor-β Hepatic fibrosis Paclitaxel smad Microtubules

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Melatonin Ameliorates Liver Fibrosis Induced by Carbon Tetrachloride in Rats via Inhibiting TGF-β1/smad Signaling Pathway

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Current Medical Science 2018年第2期38卷 236-244页

作者： Yu-rong WANG Ru-tao HONG Yuan-yuan XIE Jian-ming XU Department of Gastroenterology First Affiliated Hospital of Anhui Medical University Key Laboratory of DigestiveDisease of Anhui Province Hefei 230022 China

Melatonin has been reported to inhibit hepatic fibrosis and the mechanism may be correlated to its anti-oxidant effect. Nevertheless, the mechanism is not completely identified. This study was conducted to investigate the effects of melatonin on TGF-β1/smad signaling pathway in liver fibrosis in rats. The liver fibrosis model was made by the subcutaneous injection of CC14. The liver pathology changes were detected using hematoxylin and eosin （H＆E） staining and Van Gieson （VG） staining. Serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） activities were measured with an autoanalyzer. Glutathione peroxidase （GPx） activities and levels of malondialdehyde （MDA） and hydroxyproline （Hyp） in liver were evaluated by spectrophotometry. Expression levels of TGF-β1, smad2/3, phosphorylated smad2/3 （p-smad2/3） and smad7 in liver were detected by immunohistochemistry and Western blot analysis. Results showed that melatonin suppressed CC14-induced liver fibrosis, along with an improvement in histological changes, significant decreases in pathologic grading sores and obvious decreases in Hyp levels in liver. Melatonin improved liver function indicated by decreased serum ALT and AST activities. In addition, melatonin exerted its anti-oxidant effects, as supported by decreased MDA levels and increased GPx activities in liver. Furthermore, melatonin inhibited TGF-β1/smad pathway, as evidenced by decreased TGF-β1, smad2/3 and p-smad2/3 expression and increased smad7 expression in liver. In conclusion, melatonin may suppress CCl4-induced hepatic fibrosis in rats via inhibiting TGF-β1/smad pathway. It is possible for melatonin to be a potential reagent to treat and cure liver fibrosis.

关键词： melatonin liver fibrosis TGF-β1 smad

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Effect of Banxia Xiexin decoction on Helicobacter pylori-related peptic ulcers and its possible mechanism via the TGF-β/smad signaling pathway

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Journal of Traditional Chinese Medicine 2018年第3期38卷 419-426页

作者： Chen Shaofang Liang Huiqing Chen Shaodong Huang Yanping Wan Shichuan Huang Yanxia Department of Clinical Basis of Traditional Chinese Medicine College of Chinese Medicine Fujian University of Traditional Chinese Medicine Liver Disease Center Xiamen Hospital of Traditional Chinese Medicine Department of Traditional Chinese Medicine Medical College of Xiamen University

OBJECTIVE: To investigate the effect of Banxia Xiexin decoction(BXD) on Helicobacter pylori(Hp)-related peptic ulcers(PUs) and the possible mecha-nism underlying BXD actions via the transforming growth factor-β/small mothers against decapentaplegic(TGF-β/smad) signaling pathway.METHODS: PU patients with cold-heat complex syndrome were randomly assigned to groups that received Chinese or Western medicines with 20 patients in each group. Serum was collected after 7 d of treatment. The healthy group included 20 individuals. Gastric mucosal epithelial cell line GES-1 was cultured in vitro and randomly divided into the following seven groups: control, model, healthy,Western Medicine, prior treatment, low dosage,and high dosage. After 72 h of treatment with the corresponding serum, the m RNA and protein expression levels of TGF-β1, smad3, and smad7 were measured by reverse transcription quantitative polymerase chain reaction and western blotting, respectively.RESULTS: The m RNA expression levels of TGF-β1 and smad3 in GES-1 cells were increased after Hp introduction, and these increased levels were reduced by the BXD-containing serum. The protein levels of p-smad3, but not TGF-β1 or smad3, were significantly increased in Hp-treated GES-1 cells,and treatment with the BXD-containing serum markedly decreased the protein levels. smad7 expression was significantly enhanced following treatment with the BXD-containing serum at transcriptional and protein levels in a dose-dependent manner.CONCLUSION: BXD regulates the TGF-β/smad signaling pathway by inhibiting the expression of TGF-β1 and smad3, and increasing the expression of smad7.

关键词： Helicobacter pylori Peptic ulcer Trans-forming growth factor beta smad proteins Banxia Xiexin decoction human drug-containing serum

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Wulong Xiaozheng Wan medicated serum inhibits epithelial-mesenchymal transition in human gastric carcinoma cell line BGC823 by modulation of transforming growth factor-β1/smad signaling

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Journal of Traditional Chinese Medicine 2019年第3期39卷 380-392页

作者： Zhang Yali Wang Bingyu Guo Xueying Yang Lei Li Dandan Yuan Xingxing Department of Gastroenterology Nangang branch of Heilongjiang Academy of Traditional Chinese Medicine Harbin 150006 China Pharmacological Laboratory of Heilongjiang Academy of Traditional Chinese Medicine Harbin 150036China

OBJECTIVE:To evaluate the effect of Wulong Xiaozheng Wan medicated serum on the epithelial-mesenchymal transition (EMT) of BGC823 cell induced by transforming growth factor-β,(TGF-β,) and to explore its mechanism.METHODS:EMT model of BGC823 was stimulated by TGF-β1.Wulong Xiaozheng Wan medicated serum and LY-364947 were used as intervention.The proliferation and adhesion of BGC823 were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and flow cytometry was used to detect the apoptosis.The invasion and migration were detected by Transwell.The level of matrix metalloproteins was detected by enzyme-linked immunosorbent assay.The expressions of related proteins and mRNA of EMT marker and TGF-β1/smad signal pathway were detected by Western blot and reverse transcription-polymerase chain reaction.RESULTS:Compared with the TGF-β1 group,Wulong Xiaozheng Wan medicated serum could inhibit the ability of proliferation,heterogeneous adhesion,invasion,and migration.It also promotes apoptosis and homotypic adhesion in BGC823,with a dose-dependent manner.Meanwhile,Wulong Xiaozheng Wan medicated serum could regulate the expression of related proteins and mRNA of TGF-β1/smad signaling pathway,and inhibit the expressions of EMT transcription factors and EMT markers.CONCLUSION:Wulong Xiaozheng Wan medicated serum inhibited epithelial-mesenchymal transition by down-regulated the expression of TβRI and the activation of TGF-β1/smad signaling pathway.

关键词： Transforming growth factor beta1 smad proteins Signal transduction Epithelial-mesenchymal transition Matrix metalloproteinases,secreted BGC823 cell Wulong Xiaozheng Wan

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The role of smad signaling in vascular and hematopoietic development revealed by studies using genetic mouse models

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Science China(Life Sciences) 2010年第4期53卷 485-489页

作者： LAN Yu & YANG Xiao State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071, China State Key Laboratory of Proteomics Genetic Laboratory of Development and Diseases Institute of Biotechnology Beijing China

smads are intracellular mediators of transforming growth factor β (TGF-β) superfamily signaling. In this review, we focus on the genetic mouse models for smad pathways, which have provided functional evidence regarding the complex circuitry in angiogenesis and hematopoiesis during development. In the early stages of vascular development, TGF-β signaling is a contri buting factor in angiogenesis and vascular maturation. Whereas in the later embryogenesis, selected molecules of smad pathways, such as TGF-β type II receptor (TbRII), ALK5, and smad5, seem to be dispensable for vessel morphogenesis and integrity. TGF-β signaling is not required in the induction of hematopoietic precursors from mesoderm, but inhibits the subsequent expansion of committed hematopoietic precursors. By contrast, bone morphogenetic protein 4 (BMP4) has long been acknowledged pivotal in mesoderm induction and hematopoietic commitment during development. However, recent genetic evidence shows the BMP4-ALK3 axis is not crucial for the formation of hematopoietic cells from FLK1+ mesoderm. Because of the highly redundant mechanisms within the smad pathways, the precise role of the smad signaling involved in vascular and hematopoietic development remains nebulous. The generation of novel cell lineage restricted Cre transgenes would shed new light on the future relevant investigations.

关键词： smad transforming growth factor β (TGF-β) bone morphogenetic protein (BMP) angiogenesis hematopoiesis knockout development

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