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Cardiac fibroblast heat shock protein 47 aggravates cardiac fibrosis post myocardial ischemia-reperfusion injury by encouraging ubiquitin specific peptidase 10 dependent Smad4 deubiquitination

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Acta Pharmaceutica Sinica B 2022年第11期12卷 4138-4153页

作者： Saiyang Xie Yun Xing Wenke Shi Min Zhang Mengya Chen Wenxi Fang Shiqiang Liu Tong Zhang Xiaofeng Zeng Si Chen Shasha Wang Wei Deng Qizhu Tang Department of Cardiology Renmin Hospital of Wuhan UniversityWuhan 430060China Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan 430060China Cardiovascular Research Institute of Wuhan University Wthan 430060China

Despite complications were significantly reduced due to the popularity of percutaneous coronary intervention(PCI) in clinical trials, reperfusion injury and chronic cardiac remodeling significantly contribute to poor prognosis and rehabilitation in AMI patients. We revealed the effects of HSP47 on myocardial ischemia-reperfusion injury(IRI) and shed light on the underlying molecular mechanism.We generated adult mice with lentivirus-mediated or miRNA(mi1/133TS)-aided cardiac fibroblastselective HSP47 overexpression. Myocardial IRI was induced by 45-min occlusion of the left anterior descending(LAD) artery followed by 24 h reperfusion in mice, while ischemia-mediated cardiac remodeling was induced by four weeks of reperfusion. Also, the role of HSP47 in fibrogenesis was evaluated in cardiac fibroblasts following hypoxia-reoxygenation(HR). Extensive HSP47 was observed in murine infarcted hearts, human ischemic hearts, and cardiac fibroblasts and accelerated oxidative stress and apoptosis after myocardial IRI. Cardiac fibroblast-selective HSP47 overexpression exacerbated cardiac dysfunction caused by chronic myocardial IRI and presented deteriorative fibrosis and cell proliferation.HSP47 upregulation in cardiac fibroblasts promoted TGFβ1-Smad4 pathway activation and Smad4 deubiquitination by recruiting ubiquitin-specific peptidase 10(USP10) in fibroblasts. However, cardiac fibroblast specific USP10 deficiency abolished HSP47-mediated fibrogenesis in hearts. Moreover, blockage of HSP47 with Col003 disturbed fibrogenesis in fibroblasts following HR. Altogether, cardiac fibroblast HSP47 aggravates fibrosis post-myocardial IRI by enhancing USP10-dependent Smad4 deubiquitination,which provided a potential strategy for myocardial IRI and cardiac remodeling.

关键词： Heat shock protein 47 Myocardial ischemia-reperfusion injury Ubiquitin-specific protease 10 Cardiac fibrosis s Smad4 fibroblast Cell proliferation Cardiae dysfunction

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fibroblast-localized lncRNA CFIRL promotes cardiac fibrosis and dysfunction in dilated cardiomyopathy

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Science China Life Sciences 2024年第6期67卷 1155-1169页

作者： Shuai Yuan Xudong Zhang Jiabing Zhan Rong Xie Jiahui Fan Beibei Dai Yanru Zhao Zhongwei Yin Qian Liu Dao Wen Wang Huaping Li Chen Chen Division of Cardiology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders Department of Forensic Medicine Tongji Medical College Huazhong University of Science and Technology

CFIRL is a long noncoding RNA(lnc RNA), we previously identified as the most significantly upregulated lnc RNA in the failing hearts of patients with dilated cardiomyopathy(DCM). In this study, we determined the function of CFIRL and its role in DCM. Real-time polymerase chain reaction and in situ hybridization assays revealed that CFIRL was primarily localized in the nucleus of cardiac fibroblasts and robustly increased in failing hearts. Global knockdown or fibroblast-specific knockout of CFIRL attenuated transverse aortic constriction(TAC)-induced cardiac dysfunction and fibrosis in vivo. Overexpression of CFIRL in vitro promoted fibroblast proliferation and aggravated angiotensin II-induced differentiation to myofibroblasts. CFIRL knockdown attenuated these effects. Mechanistically, RNA pull-down assay and gene expression profiling revealed that CFIRL recruited ENO1, a newly identified noncanonical transcriptional factor, to activate IL-6transcription. IL-6 exerted a paracrine effect on cardiomyocytes to promote cardiac hypertrophy, which can be prevented by CFIRL knockdown. These findings uncover the critical role of CFIRL, a fibroblast-associated lnc RNA, in heart failure by facilitating crosstalk between fibroblasts and cardiomyocytes. CFIRL knockdown might be a potent strategy to prevent cardiac remodeling in heart failure,particularly in DCM.

关键词： lncRNA fibroblast fibrosis dilated cardiomyopathy heart failure

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Constructing Nanoscale Topology on the Surface of Microfibers Inhibits fibroblast Fibrosis

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Advanced Fiber Materials 2022年第5期4卷 1219-1232页

作者： Yongjie Jiao Xiaojing Li Jinjie Chen Chaojing Li Laijun Liu Xingxing Liu Fujun Wang Guang Chen Lu Wang Key Laboratory of Textile Science and Technology Ministry of EducationCollege of TextilesDonghua UniversityShanghai 201620China Healthcare Department of Taizhou Hospital Affiliated to Wenzhou Medical University(Zhejiang Province Taizhou Hospital) Taizhou 317000China Department of Vascular Surgery Taizhou Hospital Affiliated to Wenzhou Medical University(Zhejiang Province Taizhou Hospital)Taizhou 317000China

Fibrosis is a common problem in soft tissue regeneration,often caused by the differentiation of fibroblasts into myofibro-blasts.Because of the nanoscale topology that regulates the mechanical transduction of cells,nanofibers or nanoparticles are commonly used to modulate fibroblast differentiation.However,the strength of nanofibers is insufficient,and the physi-ological toxicity of nanoparticles still remains to be verified.In this study,self-induced crystallization was used to construct nano-protrusions on the random and aligned polycaprolactone microfibers to regulate the behavior of fibroblasts.The results revealed that the mechanical properties of microfibers with a nanoscale topology were improved.Immunofluorescence staining manifested that nano-protrusions impeded the activation of integrins and vinculins,thereby inhibiting the nuclear transfer of Yes-associated protein,resulting in a decrease in the expression ofα-smooth muscle actin.Nanoscale topology of microfibers hampered the activation of the Rho/ROCK signalling pathway.In general,we used a simple process to con-struct a fibrous scaffold with a micro-nano multilevel structure.This structure can hinder the transformation of fibroblasts into myofibroblasts on both random and aligned fibers,which is expected to prevent fibrosis.

关键词： Electrospinning Topology fibroblast Fibrosis

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fibroblast growth factor receptor 4 protein expression and clinicopathological features in gastric cancer

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World Journal of Gastroenterology 2015年第6期21卷 1838-1844页

作者： Hao Chen Dan-Ping Shen Zi-Zhen Zhang Jia-Hua Liu Yan-Ying Shen Xing-Zhi Ni Department of General Surgery Ren Ji Hospital School of Medicine Shanghai Jiao Tong University Department of Pathology Ren Ji Hospital School of Medicine Shanghai Jiao Tong University

AIM:To investigate fibroblast growth factor receptor4(FGFR4)protein expression in Chinese patients with resectable gastric cancer(GC)and the association with clinicopathological characteristics and survival.who underwent curative surgical procedures were enrolled in this study.The protein expression of FGFR4 in formalin-fixed,paraffin-embedded(FFPE)GC tissues was determined by immunohistochemical(IHC)analysis.Patient clinicopathological data and survival information were also collected andχ2 statistical analysis was performed to analyze FGFR4 protein expression in the subgroups with differing clinicopathological characteristics including;gender,age,tumor location,differentiation,tumor-node-metastasis stage,macroscopic type,depth of invasion,lymph node metastases,distant metastasis,neural invasion and vascular invasion.Furthermore,some common molecular markers of GC in our cancer center,including p53,p27,topoisomeraseⅡα(TopoⅡα)were also determined by IHC and their association with FGFR4 protein expression evaluated.The probability of survival for different subgroups with different clinicopathological characteristics was calculated using the Kaplan-Meier method and survival curves plotted using the log rank test.RESULTS:Seventy seven cases(44%)were found to have high expression of FGFR4 protein.Significantly different FGFR4 expression was observed between gastric cancers with differing expression of TopoⅡα(log rankχ2=9.4760,P=0.0236).No significant differences were observed between subgroups defined by any of the other clinicopathological characteristics.The median survival time of the FGFR4 high expression(77 cases)and low expression groups(98 cases)was27 mo and 39 mo,respectively.The five-year survival rates and median survival times of gastric cancers with high FGFR4 expression were worse than those with low expression(30.8%vs 39.2%,27 mo vs 39 mo),respectively,however,no significant difference was observed in survival time(log rankχ2=1.0477,P=0.3060).Survival analysis revealed that high expression of FGFR4 was

关键词： Gastric cancer fibroblast growth factor receptor 4

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Role of various imbalances centered on alveolar epithelial cell/fibroblast apoptosis imbalance in the pathogenesis of idiopathic pulmonary fibrosis

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Chinese Medical Journal 2021年第3期134卷 261-274页

作者： Qing Wang Zhao-Liang Xie Qi Wu Zhi-Xian Jin Chao Yang Jing Feng Department of Respiratory and Critical Care Medicine of Kunming Municipal First People’s Hospital KunmingYunnan 650000China Graduate School Tianjin Medical UniversityTianjin 300070China Respiratory Department of Sanming Yongan General Hospital SanmingFujian 366000China Medical School Tianjin University SchoolTianjin 300072China Department of Respiratory and Critical Care Medicine Tianjin Medical University General HospitalTianjin 300052China

There have been recent extensive studies and rapid advancement on the pathogenesis underlying idiopathic pulmonary fibrosis(IPF),and intricate pathogenesis of IPF has been suggested.The purpose of this study was to clarify the logical relationship between these mechanisms.An extensive search was undertaken of the PubMed using the following keywords:"etiology,""pathogenesis,""alveolar epithelial cell(AEC),""fibroblast,""lymphocyte,""macrophage,""epigenomics,""histone,"acetylation,""methylation,""endoplasmic reticulum stress,""mitochondrial dysfunction,""telomerase,""proteases,""plasminogen,""epithelial-mesenchymal transition,""oxidative stress,""inflammation,""apoptosis,"and"idiopathic pulmonary fibrosis."This search covered relevant research articles published up to April 30,2020.Original articles,reviews,and other articles were searched and reviewed for content;240 highly relevant studies were obtained after screening.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors:environmental exposures affect epigenetic marks;epigenetic processes translate environmental exposures into the regulation of chromatin;epigenetic processes shape gene expression profiles;in turn,an individual’s genetic background determines epigenetic marks;finally,these genetic and epigenetic factors act in concert to dysregulate gene expression in IPF lung tissue.The pathogenesis of IPF involves various imbalances including endoplasmic reticulum,telomere length homeostasis,mitochondrial dysfunction,oxidant/antioxidant imbalance,Th1/Th2 imbalance,M1-M2 polarization of macrophages,protease/antiprotease imbalance,and plasminogen activation/inhibition imbalance.These affect each other,promote each other,and ultimately promote AEC/fibroblast apoptosis imbalance directly or indirectly.Excessive AEC apoptosis and impaired apoptosis of fibroblasts contribute to fibrosis.IPF is likely the result of complex interactions between environmental,genetic,and epigenetic factors.The pathogenesis of IPF involves

关键词： Alveolar epithelial cell Apoptosis Idiopathic pulmonary fibrosis fibroblast Pathogenesis

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Prunella vulgaris Polysaccharide Inhibits Growth and Migration of Breast Carcinoma-Associated fibroblasts by Suppressing Expression of Basic fibroblast Growth Factor

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Chinese Journal of Integrative Medicine 2020年第4期26卷 270-276页

作者： HAO Jian DING Xiu-li YANG Xue WU Xiong-zhi Zhong-Shan-Men In-Patient Department Tianjin Medical University Cancer Institute and HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjin(300060)China Clincal Center of Tumor Therapy The Fourth Central Hospital Affiliated to Nankai UniversityTianjin(300140)China

Objective:To study the effects of Prunella vulgaris polysaccharide(PVP)on human breast carcinoma-associated fibroblasts(CAFs).Method:Cell viability was detected by 3-[4,5-dimethylthiazol-2-yl]-2,5-(3-carboxymethoxyphenyl)-2-4-sulfophenyl)?2H?tetrazolium(MTS)assay.Wound healing experiment and transwell migration assay were used to investigate the anti-migration effects.Flow cytometry was applied to detect cell apoptosis and cell cycle distribution.Reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expression of basic fibroblast growth factor(bFGF)in CAFs.Culture SKBr-3 with CAFs conditioned medium(CAFs-CM)to evaluate the indirect function on the proliferation of breast cancer SKBr-3 cells.Results:PVP inhibited the viability of CAFs by inducing apoptosis(P<0.01)and arresting cell cycle(P<0.01).It also inhibited the migration of CAFs(P<0.01).bFGF promoted CAFs proliferation(P<0.01)and migration(P<0.01),protected CAFs from apoptosis(P<0.05)and reduced Go phase to 49.06%(P<0.01).However,these effects of bFGF on CAFs could be abrogated by PVP.Culturing SKBr-3 with CAFs-CM,PVP could inhibit the viability of breast cancer SKBr-3 cells indirectly.Moreover,PVP reduced the mRNA expression(P<0.01)and protein secretion of bFGF(P<0.01)in CAFs.Conclusion:PVP could exert an anti-cancer effect on breast CAFs by inhibiting bFGF expressi on,thus inhibit!ng the growth of breast can cer SKBr-3 cells in directly.

关键词： Prunella vulgaris polysaccharide carci no ma-associated fibroblasts basic fibroblast growth factor SKBr-3 Chinese medicine

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Inhibitory Effects of Sulfur Dioxide on Rat Myocardial fibroblast Proliferation and Migration

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Chinese Medical Journal 2018年第14期131卷 1715-1723页

作者： Lu-Lu Zhang Jun-Bao Du Chao-Shu Tang Hong-Fang Jin Ya-Qian Huang Department of Pediatrics Peking University First Hospital Beijing 100034 China Division of Small Molecules and Cardiovascular Disease Key Laboratory of Molecular Cardiology Ministry of Education Beijing 100083 China Department of Physiology and Pathophysiology Peking University Health Science Centre Beijing 100091 China

Background： Myocardial fibrosis is an important pathological change has not yet been fully elucidated. The study was designed to examine fibroblast proliferation and migration inhibitor. in many heart diseases, but its pathogenesis is very complex and whether endogenous sulfur dioxide （SO2） is a novel myocardial Methods： Primary rat myocardial fibroblasts were isolated and transfected with aspartate aminotransferase （AAT1 and AAT2） knockdown lentivirus or empty lentivirus. SO2 content in the supematant was determined with high-performance liquid chromatography, and the expressions of AATI, AAT2, proliferating cell nuclear antigen （PCNA）, phosphorylated extracellular signal-regulated protein kinase （p-ERK）, and total ERK （T-ERK） in the cells were detected. Cell migration was detected by wound healing test. Independent sample t-test （for two groups） and one-way analysis of variance （three or more groups） were used to analyze the results. Results： Both AATI and AAT2 knockdown significantly reduced SO2 levels （F = 31.46, P 〈 0.01） and AATI/2 protein expression （AAT1, t = 12.67, P 〈 0.01 ; AAT2, t = 9.61, P 〈 0.01 ）, but increased PCNA expression and Cell Counting Kit-8 （CCK-8） activity as well as the migration in rat primary myocardial fibroblasts （P 〈 0.01）. Supplementation of SO： rather than pyruvate significantly inhibited the increase in proliferation and migration caused by AAT knockdown （P 〈 0.01）. Mechanistically, the ratio of p-ERK to T-ERK was significantly increased in the AAT1/2 knockdown groups compared with that in the empty lentivirus group （AATI, t = -7.36, P 〈 0.01; AAT2, t = 10.97, P 〈 0.01 ）. Whereas PD98059, an inhibitor of ERK activation, successfully blocked AAT knockdown-induced PCNA upregulation （F = 74.01, P 〉 0.05）, CCK-8 activation （F = 50.14, P 〉 0.05）, and migration augmentation in myocardial fibroblasts （24 h,F= 37.08, P〉 0.05; 48 h, F= 58.60, P〉 0.05）. Conclusion： Endogenous SO2 might be a novel myocardial fibrob/ast proliferation and migration inhibitor via inhibiting the ERK signaling

关键词： Endogenous fibroblast Migration Proliferation Sulfur Dioxide

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Mechanisms by which fibroblast growth factor 20 improves motor performance in a mouse model of Parkinson’s disease

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Neural Regeneration Research 2019年第8期14卷 1438-1444页

作者： Ai-Qin Wang Li-Na Kong Ming-Zhu Meng Xiu-He Zhao Si Chen Xiao-Tang Wang Qilu Hospital of Shandong University

Genome-wide studies have reported that Parkinson's disease is associated with abnormal expression of various growth factors. In this study, male C57BL/6 mice aged 10 weeks were used to establish Parkinson's disease models using an intraperitoneal injection of 60 mg/kg 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine. 28 days later, 10 or 100 ng fibroblast growth factor 20 was injected intracerebroventricularly. The electrophysiological changes in the mouse hippocampus were recorded using a full-cell patch clamp. Expression of Kv4.2 in the substantia nigra was analyzed using a western blot assay. Serum malondialdehyde levels were analyzed by enzyme-linked immunosorbent assay. The motor coordination of mice was evaluated using the rotarod test. The results showed that fibroblast growth factor 20 decreased A-type potassium current in neurons of the substantia nigra, increased long-term potentiation amplitude in the hippocampus, and downregulated Kv4.2 expression. A high dose of fibroblast growth factor 20 reduced serum malondialdehyde levels and enhanced the motor coordination of mice. These findings confirm that fibroblast growth factor 20 has a therapeutic effect on the toxicity induced by l-methyl-4-phenyl-l,2,3s6-tetrahydropyridine, and its mechanism of action is associated with the inhibition of A-type K^+ currents and Kv4.2 expression. All animal procedures were approved by the Animal Care and Use Committee of Qilu Hospital of Shandong University, China in 2017 (approval No. KYLL-2017-0012).

关键词： nerve regeneration Parkinson's disease l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine fibroblast growth factor 20 A-type potassium current long-term potentiation Kv4.2 oxidative stress malondialdehyde motor performance neural regeneration

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fibroblast growth factor receptor 4 single nucleotide polymorphism Gly388Arg in head and neck carcinomas

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World Journal of Clinical Oncology 2019年第3期10卷 136-148页

作者： Eva Wimmer Stephan Ihrler Olivier Gires Sylvia Streit Wolfgang Issing Christoph Bergmann Department of Otorhinolaryngology Ludwig-Maximilians-University Institute of Pathology Ludwig-Maximilians-University Clinical Cooperation Group Personalized Radiotherapy of Head and Neck Tumors Department of Molecular Biology Max-Planck-Institute for Biochemistry ENT Department Freeman Hospital Department of Otorhinolaryngology University of Duisburg-Essen

BACKGROUND Head and neck squamous cell carcinoma(HNSCC) is considered to be a progressive disease resulting from alterations in multiple genes regulating cell proliferation and differentiation like receptor tyrosine kinases(RTKs) and members of the fibroblast growth factor receptors(FGFR)-family. Singlenucleotide polymorphism(SNP) Arg388 of the FGFR4 is associated with a reduced overall survival in patients with cancers of various types. We speculate that FGFR4 expression and SNP is associated with worse survival in patients with HSNCC.AIM To investigate the potential clinical significance of FGFR4 Arg388 in the context of tumors arising in HNSCC, a comprehensive analysis of FGFR4 receptor expression and genotype in tumor tissues and correlated results with patients' clinical data in a large cohort of patients with HNSCC was conducted.METHODS Surgical specimens from 284 patients with HNSCC were retrieved from the Institute of Pathology at the Ludwig-Maximilian-University in Germany.Specimens were analyzed using immunohistochemistry and polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP). The expression of FGFR4 was analyzed in 284 surgical specimens of HNSCC using immunohistochemstry. FGFR4 polymorphism was detected by PCR-RFLP.Patients' clinical data with a minimum follow-up of 5 years were statistically evaluated with a special emphasis on survival analysis employing Kaplan-Meier estimator and Cox regression analysis.RESULTS Concerning the invasive tumor areas the intensity of the FGFR4 expression was evaluated in a four-grade system: no expression, low expression, intermediate and high expression. FGFR4 expression was scored as "high"(+++) in 74(26%),"intermediate"(++) in 103(36.3%), and "low"(+) in 107(36.7%) cases. Analyzing the FGFR4 mutation it was found in 96 tumors(33.8%), 84 of them(29.6%) having a heterozygous and 12(4.2%) homozygous mutated Arg388 allele. The overall frequency concerning the mutant alleles demonstrated 65% vs 34% mutated alleles in general. FGFR4 Arg388 was si

关键词： fibroblast growth factor receptor 4 Single-nucleotide polymorphism Head and neck squamous cell carcinoma Reduced survival Cancer progression Polymerase chain reaction Immunohistochemistry Outcome

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Effects of substance P on growth of fibroblast-like cells derived from bile duct： an in vitro cell culture study

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Chinese Medical Journal 2014年第17期127卷 3121-3126页

作者： Tian Yuanhu Yang Guangyun Zhang Xiaoqing Shen Wei Dong Jiahong Xu Zhi Department of Hepatobiliary Surgery Chinese People's Liberation Army General Hospital Beijing 100853 China Department of General Surgery Peking University Third Hospital Beijing 100191 China

Background The possible role of substance P （SP） during wound healing has been the primary research focus in recent years,but its effect on the healing process after bile duct injury is little understood.This study aimed to investigate the effects of SP on growth of fibroblast-like cells derived from rabbit bile duct.Methods fibroblast-like cells derived from rabbit bile duct were identified and divided randomly into control and experimental groups.SP-treated cells at different concentrations of 10^-9-10^-5 mol/L and control group were incubated,respectively,for 48 hours.After incubating,the effects of SP on cell proliferation were assessed by cell counts and MTT test.Apoptosis rate （AR） of cells was measured by flow cytometry.Results Cultured rabbit bile duct cells were fibroblast-like in morphology,and these cells were stained positively for vimentin and negatively for desmin.After SP was added to nonconfluent cells for 48 hours,cell numbers were significantly increased in experimental groups than in controls （P 〈0.05）.The maximum stimulation of cell proliferation was achieved at SP of 10^-5 mol/L.Bile duct fibroblast-like cells in the SP group showed a higher proliferating activity and lower AR than those in the control group or in the SP ＋ Spantide group （P 〈0.05）.Spantide partly inhibited the effects of SP on fibroblastlike cells.Examination under transmission electron microscopy revealed rough endoplasmic reticulum and prominent Golgi complexes after SP treatment.Conclusions SP has a growth regulatory property on cultivated bile duct fibroblast-like cells in vitro,suggesting that SP may involve in wound healing after bile duct injury by promoting wound fibroblast proliferation and inhibiting apoptosis and participate in pathological scar formation.

关键词： substance P bile duct fibroblast cell culture cell proliferation

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