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Sodium tanshinone ⅡA sulfonate prevents radiation-induced damage in primary rat cardiac fibroblasts

Chinese Journal of Natural Medicines 2020年第6期18卷 436-445页

作者： ZHOU Dan YANG Wen-Ke ZHANG Yi-Fan XIE Jin-Hui MA Li YANG Hui-Dong LI Yi XIE Ping Department of Cardiology Gansu Provincial HospitalLanzhou 730000China School of Clinical Medicine Gansu University of Chinese MedicineLanzhou 730000China School of Basic Medical Science Lanzhou UniversityLanzhou 730000China Ningxia Medical University Yinchuan 750004China Gansu Provincial Hospital Lanzhou 730000China School of Stomatology Lanzhou UniversityLanzhou 730000China

This study investigated the effects of X-ray irradiation on primary rat cardiac fibroblasts(CFs) and its potential mechanism, as well as whether sodium tanshinone ⅡA sulfonate(STS) has protective effect on CFs and its possible mechanism. Our data demonstrated that X-rays inhibited cell growth and increased oxidative stress in CFs, and STS mitigated X-ray-induced injury. Enzyme-linked immuno-sorbent assay showed that X-rays increased the levels of secreted angiotensin Ⅱ(Ang Ⅱ) and brain natriuretic peptide(BNP). STS inhibited the X-ray-induced increases in Ang Ⅱ and BNP release. Apoptosis and cell cycle of CFs were analyzed using flow cytometry. X-rays induced apoptosis in CFs, whereas STS inhibited apoptosis in CFs after X-ray irradiation. X-rays induced S-phase cell cycle arrest in CFs, which could be reversed by STS. X-rays increased the expression of phosphorylated-P38/P38,cleaved caspase-3 and caspase-3 as well as decreased the expression of phosphorylated extracellular signal-regulated kinase 1/2(ERK1/2)/ERK 1/2 and B cell lymphoma 2(Bcl-2)/Bcl-2 associated X protein(BAX) in CFs, as shown by Western blotting. STS mitigated the X-ray radiation-induced expression changes of these proteins. In conclusion, our results demonstrated that STS may potentially be developed as a medical countermeasure to mitigate radiation-induced cardiac damage.

关键词： Sodium tanshinone IIA sulfonate cardiac fibroblasts Radiation Oxidative Stress Apoptosis

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Lysine demethylase 5B transcriptionally regulates TREM1 in human cardiac fibroblasts

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BIOCELL 2024年第7期48卷 1105-1113页

作者： CHUNLING LIANG JING CHEN XIAOJIE CHEN WEI YAN JIE YU Department of Emergency Wangjing Hospital of China Academy of Chinese Medical SciencesBeijing100102China Department of Cardiology State Key Laboratory of Cardiovascular DiseaseFuwai HospitalNational Center for Cardiovascular DiseasesChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing100102China Department of Radiology Wangjing Hospital of China Academy of Chinese Medical SciencesBeijing100102China Department of Cardiology Wangjing Hospital of China Academy of Chinese Medical SciencesBeijing100102China

Background:A differential gene,triggering receptor expressed on myeloid cells 1(TREM1),was identiﬁed in blood sequencing datasets from myocardial infarction patients and healthy ***ﬁbrosis following myocardial infarction signiﬁcantly contributes to cardiac ***:This study aimed to unveil the intrinsic regulatory mechanism of TREM1 in myocardialﬁ***:Mimicking pathology by angiotensin II(Ang II)treatment of human cardiacﬁbroblasts(HCFs),the impacts of TREM1 knockdown on its proliferation,migration,and secretion of the pro-ﬁbrotic matrix were identiﬁ*** the Human Transcription Factor Database(HumanTFDB)website,lysine-speciﬁc demethylase 5B(KDM5B)was found to bind to the TREM1 promoter,which was further validated through luciferase reporter and chromatin immunoprecipitation(ChIP).By promoting KDM5B overexpression,its effect on the regulation of TREM1 was ***:TREM1 knockdown suppressed the proliferation,migration,and secretion of the pro-ﬁbrotic matrix in HCFs upon Ang II ***5B bound to the TREM1 promoter and upregulated its transcriptional ***,KDM5B overexpression reversed the regulation of the above cellular phenotypes by TREM1 ***:This study sheds light on the positive regulation of TREM1 by KDM5B,demonstrating their role in promoting myocardialﬁ***ﬁnding provides a theoretical foundation for understanding disease pathology and potentially advancing the development of new targeted therapies.

关键词： cardiac fibroblasts Fibrosis Myeloid cell receptor Migration Proliferation

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Transplantation of 5-azacytidine treated cardiac fibroblasts improves cardiac function of infarct hearts in rats

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Chinese Medical Journal 2010年第18期123卷 2586-2592页

作者： TANG Cheng-chun MA Gen-shan CHEN Ji-yuan Department of Cardiology Zhongda Hospital Southeast University Nanjing Jiangsu 210009 China

Background Cellular cardiomyoplasty by transplantation of various cell types has been investigated as potential treatments for the improvement of cardiac function after myocardial injury. A major barrier for the clinical application of cell transplantation is obtaining sufficiently large quantities of suitable cells. AIIogeneic cellular cardiomyoplasty may provide an alternative source of abundant, transplantable, myogenic cells by in vitro manipulation of cardiac fibroblasts using chemicals including 5-azacytidine. This study evaluated cardiomyogenic differentiation of cardiac fibroblasts, their survival in myocardial scar tissue, and the effect of the implanted cells on heart function. Methods Primary cardiac fibroblasts from neonatal rats were treated with 5-azacytidine （10 pmol/L） or control. Treatment of 5-azacytidine caused myogenic differentiation of cultured cardiac fibroblasts, as defined by elongation and fusion into multinucleated myotubes with sarcomeric structures as identified by electron microscopy, and positive immunostaining for cardiac specific proteins, troponin I and 13-myosin heavy chain （13-MHC） and the gap junction protein connexin 43. The myogenic cells （1.0x106） were transplanted into the infarcted myocardium 2 weeks after coronary artery occlusion. Results By 1 month after transplantation, the converted fibroblasts gave rise to a cluster of cardiac-like muscle cells that in the hearts occupied a large part of the scar with positive immunostaining for the myogenic proteins troponin I and 13-MHC. Engrafted cells also expressed the gap junction protein connexin 43 in a disorganized manner. There was no positive staining in the control hearts treated with injections of culture medium. Heart function was evaluated at 6 weeks after myocardial injury with echocardiographic and hemodynamic measurements. Improvement in cardiac function was seen in the hearts transplanted with the 5-azacytidine-treated cardiac fibroblasts which was absent in the hear

关键词： cardiac fibroblasts myocardial infarction transplantation 5-azacytidine

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Effect of aldosterone on the proliferation of rat cardiac fibroblasts

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TMR Integrative Medicine 2020年第20期4卷 1-6页

作者： Xue-Qing He Qi Ling Yu-Lu Li Bo-Han Qu Yi-Wei Liu Qian Xu Chengde Medical College Chengde 067000China

Objective:A cell model of cardiac fibroblasts proliferation induced by aldosterone was established to observe the effect of aldosterone on the proliferation of rat cardiac ***:Primary cardiac fibroblasts were cultured by trypsin digestion method and differential adhesion method,primary cardiac fibroblasts were sub-cultured by conventional digestion method,and the immunocytochemical assay was used to identify cardiac *** second-generation cardiac fibroblasts were randomly divided into five groups:standard control group,10-9 mol/L aldosterone(ALD1)group,10-8 mol/L aldosterone(ALD2)group,10-7 mol/L aldosterone(ALD3)group,and 10-6 mol/L aldosterone(ALD4)*** viability of fibroblast cells in each group was detected by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide ***:Vimentin staining assay showed that the cultured cells staining positive,and the purity of cultured mouse cardiac fibroblasts was 95%.The results of methyl thiazolyl tetrazolium showed that compared with the control group,the low concentration of aldosterone(10-9 mol/L)had no significant effect on the proliferation of normal cardiac *** the increase in the intensity of(10-8–10-6)mol/L,aldosterone could significantly promote the proliferation of cardiac ***,there was no significant difference in absorbance value between the aldosterone group(10-6 mol/L)and the aldosterone group(10-7 mol/L)(P>0.05).The highest concentration of aldosterone group 10-7 mol/L promoted the proliferation of cardiac the optimum concentration was 10-7 mol/***:Aldosterone can promote the spread of cardiac fibroblasts in a specific concentration range.

关键词： Aldosterone cardiac fibroblasts MTT Cell viability

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Effects of Mesenchymal Stem Cells on Matrix Metalloproteinase Synthesis of Cultured cardiac fibroblasts in Rats

Effects of Mesenchymal Stem Cells on Matrix Metalloproteinas...

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2009年浙江省心电生理与起搏学术年会

作者： Yaping WANG Jian’an WANG 浙江大学医学院附属第二医院心内科

Objective This study investigated the effects of mesenchymal stem cells(MSCs)on matrix metalloproteinase synthesis of cardiac fibroblasts(CFBs)and the *** MSCs and CFBs were from SD *** control group CFBs were cultured under hypoxic conditions for 24 hours and then the conditioned media were *** above CFBs were cocultured with MSCs in transwells for 24 hours,then inserts discarded and CFBs medium ***-

关键词： Mesenchymal stem cells cardiac fibroblasts

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Activation of β-adrenergic receptors promotes IL-6 production in cardiac fibroblasts through a PKC-dependent pathway

Activation of β-adrenergic receptors promotes IL-6 producti...

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中国病理生理学会受体、肿瘤和免疫专业委员会联合学术会议

作者： Chao Chen,Jianhai Du,Youyi Zhang Institute of Vascular Medicine,Peking University Third Hospital

Interleukin-6(IL-6),originally as a proinflammatory cytokine,has pleiotropic effects on cardiac *** the role of cardiac fibroblasts(CFs) in cardiac remodeling has been received more and more *** have previously reported that activation ofβ-adrenergic receptors(β-AR) induced IL-6 production in CFs through Gs/ adenylyl cyclase(AC)/cAMP/p38 pathway independent of protein kinase A(PKA).But the detailed molecular mechanisms remain *** utilizing various pharmacological drugs,integrating with many experimental technics such as the ELISA, immunofluorescence,Western blot *** observed isoproterenol(ISO) significantly increased protein kinase C(PKC) phosphorylation and translocation from soluble to particule ***,PKC mediated IL-6 production induced by ISO,Gs activator or cAMP ***,we demonstrated that PKC8 but not PKCα/βwas responsible for the IL-6 ***,it remains unknown how cAMP activated *** further provided evidence to support that exchange protein activated by cAMP(Epac), another direct effector of cAMP,functioned as an upstream regulator of PKCδin the *** conclusion, Gs/cAMP/Epac/PKCδpathway mediated ISO-induced IL-6 secretion in cardiac fibroblasts.

关键词： β adrenergic receptors IL-6 PKCδ cardiac fibroblasts

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Cell-derived extracellular matrix-coated silk fibroin scaffold for cardiogenesis of brown adipose stem cells through modulation of TGF-β pathway

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Regenerative Biomaterials 2020年第4期7卷 403-412页

作者： Wei Liu Yanfeng Sun Xiaohui Dong Qi Yin Huimin Zhu Siwei Li Jin Zhou Changyong Wang School of Life Science and Technology Harbin Institute of Technology92 West Dazhi StreetNan Gang DistrictHarbin 150080P.R.China Tissue Engineering Research Center Academy of Military Medical Sciences27 Taiping RoadBeijing 100850P.R.China Department of Neural Engineering and Biological Interdisciplinary Studies Institute of Military Cognition and Brain SciencesAcademy of Military Medical Sciences27 Taiping RoadBeijing 100850P.R.China Pediatric Clinical CancerThe Armed Police General Hospital69 Yongding RoadBeijing 100080P.R.China

The cell-derived extracellular matrix(ECM)-modified scaffolds have advantages of mimic tissue specificity and been thought to better mimic the native cellular microenvironment in *** derived from cardiac fibroblasts(CFs)are considered as key elements that provide a natural cell growth microenvironment and change the fate of cardiomyocytes(CMs).Here,a new hybrid scaffold is designed based on silk fibroin(SF)scaffold and CFs-derived *** were seeded on the SF scaffold for 10days culturing and decellularized to produce CFs-derived ECM-coated SF *** results showed that the cell-derived ECM-modified silk fibroin scaffold material contained collagen,laminin,fibronectin and other ECM components with myocardial-like *** to explore its effects on brown adipose stem cells(BASCs)differentiation into *** found that the CFderived ECM-coated scaffold also increased the expression of CM-specific proteins(*** troponin T and α-actinin)of ***,the b1-integrin-dependent transforming growth factor-β1 signaling pathway was also involved in the regulation of CF-derived ECM by promoting the differentiation of BASCs into ***,these findings provide insights into the bionic manufacturing of engineered cardiac tissues(ECTs)and establish a theoretical basis for the construction of ECTs.

关键词： cell-derived extracellular matrix cardiac fibroblasts brown adipose stem cells silk fibroin scaffolds

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Regulations of Thyroid Hormone on cardiac Protein Kinase C Signal Pathway in vitro

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Wuhan University Journal of Natural Sciences 2004年第4期9卷 522-526页

作者： WANGBao-hua OUYANGJing-ping LIUYong-min ZHENGHan-qiao LIYin-ping SchoolofMedicine WuhanUniversityWuhan430071HubeiChina SchoolofMedicine WuhanUniversityWuhan430071HubeiChina

The experiments were conducted to assess the influences of thyroid hormone on cardiac protein kinase C(PKC) signal pathway with cultured cardiac myocytes and fibroblasts as the models. Cells were pretreated with 1% newborn calf serum (NCS) or angiotensin II (Ang II), and then following by a triiodothyronine (T3) treatment. The PKC activity, PKCα and PKCε expressions were analyzed and compared. In 1% NCS pretreatment, T3 could inhibit PKC activity and PKCε expression in cardiac myocytes. The AngII pretreatment led to an increase of PKC activity and PKCε expression in cardiac myocytes, and an increase of PKC activity in cardiac fibroblasts. Following by T3 treatment, the increased PKC activity and PKCε expression in cardiac myocytes were markedly decreased. In conclusion, whether in 1% NCS or in Ang II pretreatment, T3 could inhibit PKC activity and PKCε expression in cardiac myocytes. Key words thyroid hormone - cardiac myocytes - cardiac fibroblasts - protein kinase C CLC number Q 572 Foundation item: Supported by the Natural Science Foundation of Hubei Province (98091)Biography: WANG Bao-hua (1974-), female, Ph. D, research direction: cardiovascular pathophysiology.

关键词： thyroid hormone cardiac myocytes cardiac fibroblasts protein kinase C

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cardiac stromal cells on stage:From dull filler to specialized actors

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BIOCELL 2022年第8期46卷 1875-1877页

作者： VITTORIO PICCHIO FRANCESCA PAGANO ISOTTA CHIMENTI Department of Medical Surgical Sciences and Biotechnologies Sapienza UniversityLatina04100Italy Institute of Biochemistry and Cell Biology National Council of Research(IBBC-CNR)Monterotondo00015Italy Mediterranea Cardiocentro Napoli80122Italy

cardiac stromal cells have faced through the years a significant evolution in their definitions concerning their phenotypes,markers,and *** are surging to key roles in physiopathology,becoming important targets to be exploited for cardiac *** this perspective,we briefly discuss their role in novel therapeutic strategies for enhancing cardiac repair and regeneration.

关键词： cardiac fibroblasts cardiac stroma cardiac repair cardiac remodeling

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Glycogen synthase kinase-3β inhibition alleviates NLRP3 inflammasome activation in myocardial infarction

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中国药理学与毒理学杂志 2019年第10期 801-802页

作者： WANG Shu-hui XU Li-na SU Xue-ling MA Yu-ran ZHANG Li-rong HAN Sheng-na School of Basic Medical Sciences Zhengzhou University

OBJECTIVE To investigate the regulatory mechanisms of glycogen synthase kinase-3β(GSK-3β)on NLRP3 inflammasome activation. METHODS We conducted myocardial infarction(MI) model in male Sprague-Dawley(SD) rat during days 2-28. An in vitro investigation was performed using new-born rat/human cardiomyocyte and fibroblast cultures under typical inflammasome stimulation and hypoxia treatment. Further identification for possibility of GSK-3β active NLRP3 inflammasomes, GSK-3β immunoprecipitation was performed from the lysate of inflammasome stimulation-treated rat neonatal fibroblasts(RCFs) with or without GSK-3β inhibitor pretreatment. RESULTS Assessments of cardiac function, histochemical and biochemical assays for cardiac tissues, as well as detection of protein and m RNA expressions in heart tissues, showed that GSK-3β inhibition remarkably improves myocardial dysfunction and prevents remodeling with parallel reduction of the parameters of NLRP3 inflammasome activation after MI. The measurement of primary rats/human cells expounded that GSK-3β inhibition reduce NLRP3 inflammasome activation happens in cardiac fibroblasts, but not in cardiomyocytes. Futhermore, GSK-3β interacts with ASC and GSK-3β inhibition reduces cytoplasmic aggregates of ASC, NLRP3 and caspase-1 formation. CONCLUSION GSK-3β directly mediates NLRP3 inflammasome activation causing cardiac dysfunction in MI.

关键词： myocardial infarction glycogen synthase kinase 3 cardiac fibroblasts NLRP3 inflammasome ASC

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