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Flagellin of Pseudomonas aeruginosa induces transforming growth factor beta 1 expression in normal bronchial epithelial cells through mitogen activated protein kinase cascades

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Chinese Medical Journal 2011年第4期124卷 599-605页

作者： YANG Jing-jing WANG Dan-dan SUN Tie-ying Department of Respiratory Diseases Peking University Fifth School of Clinical Medicine Beijing Hospital Beijing 100730China

Background Acute lung infection due to Pseudomonas aeruginosa （P. Aeruginosa） is a serious problem, especially in patients with structural lung conditions or immune compromised hosts, leading to an overwhelming threat with a high risk of morbidity and mortality. As an outcome of infection, fibrosis can be linked with chronic lung diseases. But some fibrotic manifestations, such as an irreversible decrease of lung function and fibrous bands seen on chest imaging, have been found after an acute infection with P. Aeruginosa. Fibrogenesis/remodeling resulting from acute lung infection by P.aeruginosa is rarely reported. This study was designed to explore the relation between fibrogenesis/remodeling and acute infection by P. Aeruginosa in vitro. We used flagellin protein from P. Aeruginosa, a key initiator of acute P.aeruginosa lung infection, to elucidate mechanisms by which acute lung infection with P. Aeruginosa can cause fibrogenesis/remodeling.Methods We studied the effect of flagellin from P. Aeruginosa （flagellin for short） on the transforming growth factor beta 1 （TGF-β1） and interleukin-8 （IL-8） expression, and the possible involvement of the signaling pathway, tumor necrosis factor receptor-associated factor 6 （TRAF6）/mitogen activated protein kinase （MAPK） pathway. Flagellin was purified from the P. Aeruginosa standard strain, PAO1. Normal bronchial epithelial cells BEAS-2B were challenged with different concentrations of flagellin, and cell viability assessment was performed by cell counting kit-8. BEAS-2B cells were incubated with flagellin with the specific MAPK inhibitors or TRAF6 siRNA. Cell lysates and the cultured supernatant were collected. The level of TGF-β1 and IL-8 were detected by enzyme-linked immunosorbant assay （ELISA）. Western blotting was used to detect the protein levels of MAPK signal proteins p38, c-Jun NH2-terminal kinase （JNK） and extracellular regulated kinase （ERK）.Results Expression of TGF-β1 in BEAS-2B cells was elevated by flagellin vs. Control groups （（104.3±20.8） vs.（44.6±4.4）

关键词： flagellin Pseudomonas aeruginosa transforming growth factor beta 1 mitogen activated protein kinase tumor necrosis factor receptor-associated factor 6

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Follistatin-Like 1 Promotes Bleomycin-lnduced Pulmonary Fibrosis through the transforming growth factor beta 1/Mitogen-Activated Protein Kinase Signaling Pathway

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Chinese Medical Journal 2018年第16期131卷 1917-1925页

作者： Yan-Kun Jin Xiao-He Li Wang Wang Jie Liu Wei Zhang Yin-Shan Fang Zhi-Fei Zhang Hua-Ping Dai Wen Ning Chen Wang Department of Respiratory and Critical Care Medicine Beijing Chao-Yang Hospital Capital Medical University Beijing 100020 China Department of Respiratory Disease Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders Capital Medical University Beijing 100020 China Department of Respiratory Disease Capital Medical University Beijing 100020 China Department of Life Sciences State Key Laboratory of Medicinal Chemical Biology College of Life Sciences Nankai University Tianjin 300071 China Department of Physiology and Pathophysiology Capital Medical University Beijing 100069 China

Background： Follistatin-like I （FSTL 1） is a novel profibrogenic factor that induces pulmonary fibrosis （PF） through the transforming growth factor-beta 1 （TGF-[B 1 ）/Smad signaling. Little is known about its effects on PF through the non-Smad signaling, like the mitogen-activated protein kinase （MAPK） pathway. Therefore, this study aimed to investigate the role ofFSTL 1 in PF through the MAPK signaling pathway and its mechanisms in lung fibrogenesis. Methods： PF was induced in Fstll~ and wild-type （WT） C57BL/6 mice with bleomycin. After 14 days, the mice were sacrificed, and lung tissues were stained with hematoxylin and eosin; the hydroxyproline content was measured to confirm PF. The mRNA and protein level of FSTLI and the change of MAPK phosphorylation were measured by quantitative polymerase chain reaction and Western blotting. The effect of Fst11 deficiency on fibroblasts differentiation was measured by Western blotting and cell immunofluorescence. MAPK signaling activation was measured by Western blotting in Fst11＋/ and WT fibroblasts treated with recombinant human FSTLI protein. We pretreated mouse lung fibroblast cells with inhibitors of the extracellular signal-regulated kinase （ERK）, p38, and Jun N-terminal kinase （JNK） signaling and analyzed their differentiation, proliferation, migration, and invasion by Western blotting, 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide analysis, and transwell assays. The Student＇s t-test was used to compare the differences between two groups. Results： Fstll deficiency attenuated phosphorylation of the ERK, p38, and JNK signaling in bleomycin-induced fibrotic lung tissue 14 days after injury （0.67 ± 0.05 vs. 1.22 ± 0.03, t = 14.92, P = 0.0001; 0.41 ± 0.01 vs. 1.15 ± 0.07; t = 11.19; P = 0.0004; and 0.41 ± 0.01 vs. 1.07± 0.07, t = 8.92, P = 0.0009; respectively）, compared with WT lungs at the same time and in primary lung fibroblasts （0.82 ± 0.01 vs. 1.01 ±0.04, t = 4.06, P = 0.0150; 1.04 ±0.03 vs. 1.24 ± 0.03, t= 4.44, P = 0.0100： and 0.76 ±0.05 vs. 0.99±

关键词： Follistatin-Like 1 Mitogen-Activated Protein Kinase Pulmonary Fibrosis transforming growth factor beta 1

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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 (Pbeta 1 concentration reached 10 ng/ml, the expression of p-Smad3, Smad3, and Smad7 was inhibited (Pbeta 1 promotes the expression of Smad3 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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Effects of Qingguang'an(青光安)containing serum on the expression levels of autophagy-related genes in human Tenon's fibroblasts induced by transforming growth factor beta 1

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Journal of Traditional Chinese Medicine 2021年第2期41卷 236-245页

作者： YU Juan XIA Fei LI Xiang PENG Qinghua Ophthalmology Department the First Affiliated HospitalHunan University of TCMChangsha 410007China Eye Research Centre Hunan University of Traditional Chinese MedicineChangsha 410208China Hunan Provincial Key Laboratory for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine Changsha 410208China

OBJECTIVE:To explore the effects of Qingguang'an(青光安)containing serum on the expression levels of autophagy related genes in the transforming growth factor beta 1(TGF-β1)-activated human Tenon's fibroblasts(HTFs).METHODS:(a)Primary HTFs were stimulated by TGF-β1 and underwent immunohistochemistry,which established a cell model after Glaucoma filtration surgery(GFS).(b)The cell models were divided into 4 group:normal group(normal cells),model group(+TGF-β1),treatment group(+TGF-β1+medicated serum),and positive control group(TGF-β1+rapamycin).Then,Qingguang'an medicated serum with optimum concentration was added to the corresponding group.The autophagy positive cells were identified by the Cyto-ID autophagy detection kits under fluorescent microscope and Cytation 5 multifunctional instrument for cell imaging.And the mean fluorescence intensity of autophagy positive cells was determined by flow cytometry.The expression levels of autophagy related genes—Beclin-1,autophagy related gene 5(ATG-5),and microtubule-associated protein 1 light chain 3(LC-3Ⅱ)were detected by quantitative reverse transcription-polymerase chain reaction and Western blot analysis.RESULTS:Compared with the normal group and the model group,the relative mRNA expression levels of autophagy-related genes(Beclin-1,ATG-5 and LC-3Ⅱ)in the experimental group were notably increased(P1),and with the extension of treatment time,it had an increasing trend(48 h was more obvious),which showed a certain time dependency;the protein expression levels of autophagy-related genes(Beclin-1,ATG-5,and LC-3Ⅱ)were significantly increased in the experimental group(P1).With the prolongation of treatment time,there was an increasing trend(48 h was relatively obvious),and it revealed a certain time dependency CONCLUSION:The Qingguang'an medicated serum could up-regulate autophagy related genes(Beclin1,ATG5,and LC3Ⅱ)in the TGF-β1-activated HTFs.

关键词： Qingguang'an medicated serum transforming growth factor beta 1 beclin-1 autophagy-related protein 5 microtubule-associated proteins Human Tenon's fibroblasts

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transforming growth factor-β1 short hairpin RNA inhibits renal allograft fibrosis

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Chinese Medical Journal 2011年第5期124卷 655-663页

作者： YIN Zhi-kang WU Xiao-hou XIA Yu-guo LUO Chun-li Department of Urology First Affiliated Hospital Chongqing Medical University Chongqing 400016 China Faculty of Laboratory Medicine Chongqing Medical University Chongqing 400016 China

Background transforming growth factor-β1 （TGF-β1） is known to be a key fibrogenic cytokine in a number of chronic fibrotic diseases, including chronic allograft nephropathy. We examined the effects of inhibition of TGF-β1 expression by RNA interference on renal allograft fibrosis, and explored the mechanisms responsible for these effects. Methods A Sprague-Dawley-to-Wistar rat model of accelerated kidney transplant fibrosis was used. Sixty recipient adult Wistar rats were randomly divided into four groups： group J （sham-operated group）, group T （plasmid-transfected group）, group H （control plasmid group）, and group Y （transplant only group）. Rats in group T were transfected with 200 μg of TGF-β1 short hairpin RNA （shRNA）. Reverse transcription-polymerase chain reaction and Western blotting were used to examine the expression of TGF-β1, Smad3/7, E-cadherin, and type I collagen. The distribution of type I collagen was measured by immunohistochemistry. The pathologic changes and extent of fibrosis were assessed by hematoxylin and eosin and Masson staining. E-cadherin and α-smooth muscle actin immunohistochemical staining were used to label tubular epithelial cells and fibroblasts, respectively.Results Plasmid transfection significantly inhibited the expression of TGF-β1, as well as that of its target gene, type I collagen （P 〈0.05 and P 〈0.01, respectively）. In addition, the degree of fibrosis was mild, and its development was delayed in plasmid-transfected rats. In contrast, TGF-β1-shRNA transfection maintained the expression of E-cadherin in tubular epithelial cells while it inhibited the transformation from epithelial cells to fibroblasts. Blood urea nitrogen and serum creatinine were lower in the plasmid group than in the control groups （P 〈0.05 and P 〈0.01, respectively）. Conclusions This study suggests that transfection of a TGF-pl-shRNA plasmid could inhibit the fibrosis of renal allografts. The mechanism may be associated with the downregulation of Smad3 and upregulation of Smad7, resulting in suppressed epi

关键词： fibrosis gene therapy kidney transplantation RNA interference transforming growth factor beta 1

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Effect of basic fibroblast growth factor and transforming growth factor β1 on the healing of reconstructed dura by carbon dioxide laser soldering in minipigs

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Chinese Medical Journal 2012年第4期125卷 611-616页

作者： ZHONG Hong-liang WANG Zhen-min YANG Zhi-jun ZHAO Fu WANG Bo WANG Zhong-cheng LIU Pi-nan Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Beijing 100050 China Beijing Neurosurgical Institute Beijing 100050 China Department of Neurosurgery Beijing Tiantan Hospital Capital Medical University Beijing 100050 China Beijing Neurosurgical Institute Beijing 100050 China

Background Carbon dioxide （CO2） laser soldering is an alternative technique for tissue bonding.Basic fibroblast growth factor （bFGF） and transforming growth factor β1 （TGFβ1） are two key factors for wound healing.This study was performed to demonstrate the efficacy of CO2 laser soldering for dural reconstruction and the effect of bFGF and TGFβ1 on healing.Methods In Part Ⅰ,10 minipigs were randomized into two equal groups.Dural defects were reconstructed by conventional fibrin glue bonding （group Ⅰa） or CO2 laser soldering （group Ⅰb）.The reconstructed dura was subjected to burst pressure （BP） measurement and immunohistochemical staining after 1 week.In Part Ⅱ,36 minipigs were randomized into three equal groups.Dural reconstruction was achieved by CO2 laser soldering.Exogenous bFGF （group Ⅱb） or TGFβ1 （group Ⅱc） was administered while group Ⅱa served as a control group.The specimens were subjected to BP measurement after 1,2,3,and 4 weeks,respectively.Results In Part Ⅰ,the dura specimens displayed positive staining of only bFGF in group la and of both bFGF and TGFβ1 in group lb.Group Ⅰb showed higher BP than group la （（98.00-±21.41） mmHg vs.（70.80±15.09） mmHg,respectively; P 〈0.05）.In Part Ⅱ,BP of group Ⅱc was significantly higher than that of group Ⅱla （P 〈0.01）.The BP of group Ⅱa trended toward stabilization after 3 weeks of growth,while that of groups lⅡb and Ⅱc trended toward stabilization after 2 weeks of growth.Conclusions CO2 laser soldering is a reliable technique for dural reconstruction.The superior healing of dural reconstruction by CO2 laser soldering may be related to higher expression of bFGF and TGFβ1,and CO2 lasers may stimulate their secretion.Exogenous bFGF or TGFβ1 may improve healing by shortening the wound healing time,and exogenous TGFβ1 may improve the tensile strength.

关键词： basic fibroblast growth factor CO2 lasers dura mater porcine skull base reconstruction transforming growth factor beta 1

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Danggui Buxue Tang ameliorates bleomycin-induced pulmonary fibrosis in rats through inhibiting transforming growth factor-β1/Smad3/plasminogen activator inhibitor-1 signaling pathway

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Journal of Traditional Chinese Medicine 2020年第2期40卷 236-244页

作者： Wang Jiepeng Fang Chaoyi Wang Shaoxian Fang Fang Chu Xinqiao Liu Na Lu Chenxi Wang Shuo Li Wei School of Preclinical Medicine Hebei University of Chinese MedicineShijiazhuang 050200China Hebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease Hebei University of Chinese MedicineShijiazhuang 050091China

OBJECTIVE: To investigate the effect of Danggui Buxue Tang(DBT), a decoction from Traditional Chinese Medicine, on bleomycin-induced pulmonary fibrosis in rats, and to propose the possible underlying mechanism.METHODS: Forty male Sprague-Dawley rats were randomly divided into sham group, model group,prednisone group and DBT group. Pulmonary fibrosis rat model was established by intratracheal injection with bleomycin. Body weight and lung index were monitored. Histopathologic examination and collagen deposition were determined using Hematoxylin and eosin(HE) and Masson's trichrome staining. Immunohistochemistry staining was applied to observe the expression of alpha-smooth muscle actin(α-SMA). m RNA expression of α-SMA,collagen Ⅰ and collagen Ⅲ were measured by realtime fluorescence quantitative PCR(RT-q PCR). Inflammatory cytokines, including tumor necrosis factor alpha(TNF-α), interleukin-6(IL-6) and IL-1β in serum were detected by Enzyme-linked immunosorbent assay. Alkali hydrolysis method was conducted to investigate the content of hydroxyproline(HYP). transforming growth factor-β1(TGF-β1),Smad3 and plasminogen activator inhibitor-1(PAI-1) protein level were examined by Western blot assay.RESULTS: DBT significantly reduced the severity of bleomycin-induced pulmonary fibrosis and inflammation as indicated by minimizing the lost of weight, and by lowering the levels of lung index, inflammation score, Ashcroft score, collagen volume fraction(%), HYP, α-SMA, collagen Ⅰ, collagen Ⅲ,TNF-α, IL-6, IL-1β, TGF-β1, Smad3 and PAI-1, consistent with the effect of prednisone.CONCLUSION: Our findings suggest that DBT is able to ameliorate the pulmonary fibrosis, the possible mechanism may involve inhibition of pulmonary inflammation and collagen deposition, possibly via suppressing TGF-β1/Smad3/PAI-1 signaling pathway.

关键词： Pulmonary fibrosis transforming growth factor beta 1 Smad3 protein Plasminogen inactivators Danggui Buxue Tang

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Effects of insulin-like growth factor binding protein-related protein 1 in mice with hepatic fibrosis induced by thioacetamide

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Chinese Medical Journal 2010年第18期123卷 2521-2526页

作者： LIU Li-xin ZHANG Hai-yan ZHANG Qian-qian GUO Xiao-hong Experimental Center of Science and Research of the First Teaching Hospital of Shanxi Medical University Institute of Liver Disease and Key Laboratory of Cell Physiology Provincial Department of the Ministry of Education of Shanxi Medical University Taiyuan Shanxi 030001 China

Background Insulin-like growth factor binding protein-related protein 1 （IGFBPrP1） can activate hepatic stellate cells and increase extracellular matrix （ECM） in vitro. However, the effects of IGFBPrP1 in mice with hepatic fibrosis, and the mechanisms of these effects, are currently unknown. We aim to address these issues in this study. Methods Intraperitoneal injection of thioacetamide （TAA） is a classic method for establishing a mouse model of hepatic fibrosis. Using this model, we administered anti-IGFBPrP1 antibody, again via intraperitoneal injection. The morphological changes of liver fibrosis were observed with both HE and Masson stainning. The immunohistochemical assays and Western blotting were used to measure changes in IGFBPrP1, a-smooth muscle actin （a-SMA） and ECM in liver tissues, and the expression of transforming growth factor-β1 （TGF-β1） and Smad3. Data were statistically analyzed using one-way analysis of variance （ANOVA）, the SNK-q test for inter-group differences. Results The Masson staining analysis showed that compared with normal control group, content of collagen fiber in TAA5w group was significantly increased （P 〈0.01）, and it was significantly decreased in TAA5w/alGFBPrP1 group compared with in TAA5w group （P 〈0.01）. The expression of hepatic IGFBPrP1, a-SMA, TGF-β1, Smad3, collagen 1 and fibronectin （FN） was significantly up-regulated in the TAA5w group （P 〈0.01）. Anti-IGFBPrP1 treatment reversed these changes （P 〈0.01）. Conclusions IGFBPrP1 plays an important role in the development of hepatic fibrosis. Anti-IGFBPrP1 prevents fibrosis in mice by suppressing the activation of hepatic stellate cells, inhibiting the synthesis of major components of the ECM （namely, collagen I and FN）. The mechanism for this suppression of fibrosis is associated with the TGF-β1/Smad3 signaling pathways.

关键词： insulin-like growth factor binding protein-related protein 1 hepatic fibrosis extracellular matrix Smad3 protein transforming growth factor beta 1

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The Physiopathological Crossroads of Aging

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Journal of Biosciences and Medicines 2019年第6期7卷 102-128页

作者： J.Lasierra-Cirujeda P.Coronel M.J.aza pascual-salcedo M.Gimeno M.M.Aza Pascual Salcedo A.Lasierra-Ibanez C.Lasala-Aza logrono(la rioja) spain tedec-meji farma saalcala de henaresmadridspain pharmacy service la rioja health departmentla riojaspain pharmacy service aragon health servicezaragozaspain sciences faculty grade biochemistryuniversity of navarranavarraspain pharmacy faculty university of valenciavalenciaspain

Stress, inflammation and Plasminogen activator inhibitor 1 (PAI-1) are key mechanisms throughout the development of aging, constituting a crossroad in the most frequent pathologies that accompany it. Among metabolic processes, obesity, metabolic syndrome and type 2 diabetes mellitus are included and Alzheimer’s disease among the neurodegenerative processes. Stress is a mechanism of defense of the organism against exogenous and endogenous actions called stressors. In the case of low intensity stimuli, the organism responds with actions aimed at a physiological adaptation (Homeostasis). On the other hand, when a high intensity (experimental level) or chronic stimulus (oxidative stress) is repeated, structural and functional changes are observed in different organs with activation of the hypothalamus-pituitary-adrenal axis, the renin angiotensin system and the sympathetic nervous system, stimulating the production of hormones that release cytokines with proin-flammatory/antiinflammatory properties that play an important role in the previously mentioned pathologies, as well as a marked increase in PAI-1, a gene regulated by stress and by cytokines, with manifest action at the origin of thromboembolic disease, so frequent in aging. The objective of this review is to highlight the importance of the binomial stress and PAI-1 in aging and in the pathologies that accompany it. Because PAI-1 is part of the pathology and complications in aging, some authors suggest the study of PAI-1 inhibitors to achieve its physiological levels, as part of the treatment of these diseases.

关键词： Aging. Oxidative Stress Plasminogen Activator Inhibitor 1 transforming growth factor beta 1 Glutathione Alzheimer’s Disease

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