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cardiac fibroblast-Specific Activating Transcription Factor 3 Promotes Myocardial Repair after Myocardial Infarction

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Chinese Medical Journal 2018年第19期131卷 2302-2309页

作者： Yu-Lin Li Wen-Jing Hao Bo-Ya Chen Jing Chen Guo-Qi Li Key Laboratory of Remodeling-Related Cardiovascular Disease (Ministry of Education) Beijing Anzhen Hospital Affiliated to Captital Medical University Beijing Institute of Heart Lung and Blood Vessel Diseases Beijing 100029 China

Background：Myocardial ischemia injury is one of the leading causes of death and disability worldwide.cardiac fibroblasts （CFs） have central roles in modulating cardiac function under pathophysiological conditions.Activating transcription factor 3 （ATF3） plays a self-protective role in counteracting CF dysfunction.However,the precise function of CF-specific ATF3 during myocardial infarction （MI） injury/repair remains incompletely understood.The aim of this study was to determine whether CF-specific ATF3 affected cardiac repair after MI.Methods：Fifteen male C57BL/6 wild-type mice were performed with MI operation to observe the expression of ATF3 at 0,0.5,1.0,3.0,and 7.0 days postoperation.Model for MI was constructed in ATF3TGfl/flColla2-Cre＋（CF-specific ATF3 overexpression group,n =5） and ATF3TGfl/flColla2-Cre-male mice （without CF-specific ATF3 overexpression group,n =5）.In addition,five mice of ATF3TGfl/flCol1a2-Cre＋ and ATF3TGfl/flCol 1 a2-Cre-were subjected to sham MI operation.Heart function was detected by ultrasound and left ventricular remodeling was observed by Masson staining （myocardial fibrosis area was detected by blue collagen deposition area） at the 28th day after MI surgery in ATF3TGfl/flColla2-Cre＋ and ATF3TGfl/flColla2-Cre-mice received sham or MI operation.Quantitative real-time polymerase chain reaction （qRT-PCR） was used to detect cell proliferation/cell cycle-related gene expression in cardiac tissue.BrdU staining was used to detect fibroblast proliferation.Results：After establishment of an MI model,we found that ATF3 proteins were increased in the heart of mice after MI surgery and dominantly expressed in CFs.Genetic overexpression of ATF3 in CFs （ATF3TGfl/flCol1a2-Cre＋ group） resulted in an improvement in the heart function as indicated by increased cardiac ejection fraction （41.0% vs.30.5%,t =8.610,P =0.001） and increased fractional shortening （26.8% vs.18.1%,t =7.173,P =0.002）,which was accompanied by a decrease in cardiac scar area （23.1% vs.11.0%,t =8.610,P =0.001）.qRT-PCR analysis of

关键词： Activating Transcription Factor 3 cardiac fibroblast Myocardial Infarction Proliferation

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Compensatory function of bradykinin B1 receptor in the inhibitory effect of captopril on cardiomyocyte hypertrophy and cardiac fibroblast proliferation in neonatal rats

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Chinese Medical Journal 2008年第13期121卷 1220-1225页

作者： ZOU Jun REN Jiang-hua FENG Dan WANG Hong XU Jiang Department of Cardiology Zhongnan Hospital of Wuhan University Wuhan Hubei 430071 China Department of Physiology Medical College of Wuhan University Wuhan Hubei 430071 China

Background Bradykinin （BK） acts mainly on two receptor subtypes： B1 and B2, and activation of B2 receptor mediates the most well-known cardioprotective effects of angiotensin converting enzyme inhibitors （ACEi）, however, the role that B1 receptor plays in ACEi has not been fully defined. We examined the role of B1 receptor in the inhibitory effect of ACE inhibitor captopril on rat cardiomyocyte hypertrophy and cardiac fibroblast proliferation induced by angiotensin Ⅱ （Ang Ⅱ） and explored its possible mechanism. Methods Neonatal cardiomyocytes and cardiac fibroblasts （CFs） were randomly treated with Ang Ⅱ, captopdl, B2 receptor antagonist （HOE-140） and B1 receptor antagonist （des-Arg^10, Leu^9-kallidin） alone or in combination. Flow cytometry was used to evaluate cell cycle, size and protein content. Nitric oxide （NO） and intracellular cyclic guanosine monophosphate （cGMP） level were measured by colorimetry and radioimmunoassay. Results After the CFs and cardiomyocytes were incubated with 0.1 μmol/L Ang Ⅱ for 48 hours, the percentage of CFs in the S stage, cardiomyocytes size and protein content significantly increased （both P 〈0.01 vs control）, and these increases were inhibited by 10 μmol/L captopril. However, NO and cGMP levels were significantly higher than that with Ang Ⅱ alone （both P 〈0.01）. 1 μmol/L HOE-140 or 0.1 pmol/L des-Arg^10, Leu^9-kallidin attenuated the effects of captopril, which was blunted further by blockade of both B1 and B2 receptors. Conclusions Acting via B2 receptor, BK contributes to the antihypertrophic and antiproliferative effects of captopril on cardiomyocytes and CFs. In the absence of B2 receptor, B1 receptor may act a compensatory mechanism for the B2 receptor and contribute to the inhibition of cardiomyocyte hypertrophy and CFs proliferation by captopril. NO and cGMP play an important role in the effect of B1 receptor.

关键词： bradykinin captopril cardiac fibroblast cardiomyocyte

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Distinct mononuclear diploid cardiac subpopulation with minimal cell-cell communications persists in embryonic and adult mammalian heart

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Frontiers of Medicine 2023年第5期17卷 939-956页

作者： Miaomiao Zhu Huamin Liang Zhe Zhang Hao Jiang Jingwen Pu Xiaoyi Hang Qian Zhou Jiacheng Xiang Ximiao He Department of Physiology School of Basic MedicineTongji Medical College`Wuhan430030China Center for Genomics and Proteomics Research School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Hubei Key Laboratory of Drug Target Research and Pharmacodynamic Evaluation Huazhong University of Science and TechnologyWuhan430030China

A small proportion of mononuclear diploid cardiomyocytes(MNDCMs),with regeneration potential,could persist in adult mammalian heart.However,the heterogeneity of MNDCMs and changes during development remains to be illuminated.To this end,12645 cardiac cells were generated from embryonic day 17.5 and postnatal days 2 and 8 mice by single-cell RNA sequencing.Three cardiac developmental paths were identified:two switching to cardiomyocytes(CM)maturation with close CM–fibroblast(FB)communications and one maintaining MNDCM status with least CM–FB communications.Proliferative MNDCMs having interactions with macrophages and non-proliferative MNDCMs(non-pMNDCMs)with minimal cell–cell communications were identified in the third path.The non-pMNDCMs possessed distinct properties:the lowest mitochondrial metabolisms,the highest glycolysis,and high expression of Myl4 and Tnni1.Single-nucleus RNA sequencing and immunohistochemical staining further proved that the Myl4^(+)Tnni1+MNDCMs persisted in embryonic and adult hearts.These MNDCMs were mapped to the heart by integrating the spatial and single-cell transcriptomic data.In conclusion,a novel non-pMNDCM subpopulation with minimal cell–cell communications was unveiled,highlighting the importance of microenvironment contribution to CM fate during maturation.These findings could improve the understanding of MNDCM heterogeneity and cardiac development,thus providing new clues for approaches to effective cardiac regeneration.

关键词： mononuclear diploid cardiomyocytes cell-cell communication cardiac fibroblast single-cell RNA sequencing cardiac regeneration

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Calcitriol Suppressed Isoproterenol-induced Proliferation of cardiac fibroblasts via Integrinβ3/FAK/Akt Pathway

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Current Medical Science 2023年第1期43卷 48-57页

作者： Xin-feng WANG Qian LI Xia SUN Li-ming ZHENG Shao-li CHENG Yan-he ZHU Department of Physiology and Pathophysiology School of Basic Medical SciencesXi’an Jiaotong University Health Science CenterXi’an710061China Department of Ultrasound the Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’an710004China Basic Medical Experimental Teaching Center School of Basic Medical SciencesXi’an Jiaotong University Health Science CenterXi’an710061China Institute of Endemic Diseases School of Public HealthXi’an Jiaotong University Health Science CenterXi’an710061China

Objective cardiac fibroblasts(CFs)proliferation and extracellular matrix deposition are important features of cardiac fibrosis.Various studies have indicated that vitamin D displays an anti-fibrotic property in chronic heart diseases.This study explored the role of vitamin D in the growth of CFs via an integrin signaling pathway.Methods MTT and 5-ethynyl-2′-deoxyuridine assays were performed to determine cell viability.Western blotting was performed to detect the expression of proliferating cell nuclear antigen(PCNA)and integrin signaling pathway.The fibronectin was observed by ELISA.Immunohistochemical staining was employed to evaluate the expression of integrinβ3.Results The PCNA expression in the CFs was enhanced after isoproterenol(ISO)stimulation accompanied by an elevated expression of integrin beta-3(β3).The blockade of the integrinβ3 with a specific integrinβ3 antibody reduced the PCNA expression induced by the ISO.Decreasing the integrinβ3 by siRNA reduced the ISO-triggered phosphorylation of FAK and Akt.Both the FAK inhibitor and Akt inhibitor suppressed the PCNA expression induced by the ISO in the CFs.Calcitriol(CAL),an active form of vitamin D,attenuated the ISO-induced CFs proliferation by downregulating the integrinβ3 expression,and phosphorylation of FAK and Akt.Moreover,CAL reduced the increased levels of fibronectin and hydroxyproline in the CFs culture medium triggered by the ISO.The administration of calcitriol decreased the integrinβ3 expression in the ISO-induced myocardial injury model.Conclusion These findings revealed a novel role for CAL in suppressing the CFs growth by the downregulation of the integrinβ3/FAK/Akt pathway.

关键词： vitamin D cardiac fibroblast proliferation integrin myocardial fibrosis

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All-trans retinoic acid inhibited angiotensin Ⅱ-induced increase in cell growth and collagen secretion of neonatal cardiac fibroblasts

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Acta Pharmacologica Sinica 2006年第4期27卷 423-429页

作者： Yan HE~2 Ying HUANG~2 Li ZHOU~2 Li-min LU~2 Yi-chun ZHU~2 Tai YAO~(2,3,4) ~2Department of Physiology and Pathophysiology,and ~3State Key Laboratory for Medical Neurobiology.Fudan University Shanghai Medical College.Shanghai 200032.China Department of Physiology and Pathophysiology Fudan University Shanghai Medical College Shanghai China State Key Laboratory for Medical Neurobiology Fudan University Shanghai Medical College Shanghai China

Aim:To determine whether all-trans retinoic acid(atRA)acts to modulate angio-tensin Ⅱ(Ang Ⅱ)-induced cardiac fibroblast cell growth and collagen secretion.Methods:Cultured neonatal rat cardiac fibroblasts(CF)were used in the experiment.A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT)assay wasused to detect cell growth of the CF;and immunocytochemistry and Westernblotting were used to measure the production and secretion of collagen and theexpression of transforming growth factor-β1(TGF-β1)by the CF.Results:atRA(1×10-7to 1×10-5mol/L)inhibited the Ang Ⅱ-induced increase in cell growth of CF(Pcardiac remodeling.

关键词： cardiac fibroblast angiotensin Ⅱ all-trans retinoic acid collagen secretion transforming growth factor-β1

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Long non-coding RNAs in cardiac fibrosis:Regulation of cardiac fibroblasts

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South China Journal of Cardiology 2020年第4期21卷 292-303页

作者：黄思慧陈果何旭瑜余丹青 Department of Cardiology Guangdong Cardiovascular Institute Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention Guangdong Provincial People's Hospital Guangdong Academy of Medical Sciences The Second School of Clinical Medicine Southern Medical University

Background cardiac fibrosis,characterized by excessive extracellular matrix(ECM)deposition and increased cardiac fibroblasts(CFs)activity,is a common pathology of various cardiovascular diseases.cardiac fibrosis decreases ventricular compliance,increases diastolic filling pressure,decreases cardiac oxygen supply,and ultimately impairs the cardiac output.CFs are the main effecter cell type in regulating ECM and predominantly drive the fibrosis process.Despite the critical importance of CFs,our limited understanding of CFs impedes the development of potential therapies that effectively target this cell type and its pathological contribution to disease progression.Recently,long non-coding RNAs(lncRNAs)are emerging as important pathological and physiological regulators of cardiac fibrosis,shedding light on novel molecular mechanisms and potential therapeutic targets.This review discussed the current knowledge regarding the lnc RNAs involved in cardiac fibrosis and summarized their possible molecular mechanisms with special focus on the regulation of CFs.

关键词： long non-coding RNAs cardiac fibrosis cardiac fibroblast

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Macrophage migration inhibitory factor suppresses angiotensinⅡ-induced expression of fibrosis-associated genes by inactivating Smad3 and activating Nrf2 in cardiac fibroblasts

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South China Journal of Cardiology 2017年第4期18卷 312-319页

作者：肖珍邹笑朱杰宁梁景南林秋雄邓春玉杨敏符永恒薛玉梅吴书林单志新 Guangdong Cardiovascular Institute Guangdong Provincial Key Laboratory of Clinical Pharmacology Guangdong General Hospital Guangdong Academy of Medical Sciences Shantou University Medical College Shantou University

Background Macrophage migration inhibitory factor （MIF） is a key pro-inflammatory cytokine, exhibiting antioxidant properties. However, the role of MIF in cardiac fibrosis is not well known. In the present study, the effects of MIF on Smad3 and Nrf2 signalings in cardiac fibroblasts were investigated. Methods cardiac fibroblasts were isolated from 1-3 days old C57BL/6 mice, and the cardiac fibroblasts from passage 2 to 4 were used in this study. Expression of fibrosis-associated Collal, Col3al and oL-SMA in mouse cardiac fibroblasts was de- tected by immunofluorescence staining and Western-blot assay, respectively. Intracellular oxidants in mouse car- diac fibroblasts were measured by using the probe dichlorofluoroscindiacetate （DCFH-DA） under confocal mi- croscopy. Western-blot assay was also used to detect Smad3 and Nrf2, antioxidant proteins, MLL and HCF-1 in mouse cardiac fibroblasts. Results Immunofluorescence staining and Western- blot assay showed that MIF could markedly inhibit fibrosis-associated Collal, Col3al and oL-SMA expression in cardiac fibroblasts. DCFH- DA staining revealed that MIF can efficiently decrease reactive oxygen species （ROS） level in Ang-II-induced cardiac fibroblasts. Additionally, Smad3 activation was inhibited, but transcription factor Nrf2 and the downstream antioxidant genes, including HO-1, SOD-l, SOD2, Trx-2 and e-NOS, were increased in MIF-treated cardiac fibroblasts. MLL and HCF-lwere up-regulated by MIF, and either MLL knockdown or HCF-1 knock- down could consistently suppress Nrf2 expression in cardiac fibroblasts. Conclusions MIF possesses anti-fibro- sis effect by inactivating Smad3 and activating Nrf2 in cardiac fibroblasts.

关键词： macrophage migration inhibitory factor cardiac fibrosis Nrf2 Smad3 cardiac fibroblast

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