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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 HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders Wuhan 430030China Department of Forensic Medicine Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

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

Hyperglycemic memory in diabetic cardiomyopathy

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Frontiers of Medicine 2022年第1期16卷 25-38页

作者： Jiabing Zhan Chen Chen Dao Wen Wang huaping li Division of Cardiology Department of Internal MedicineTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders Wuhan 430030China

Cardiovascular diseases account for approximately 80%of deaths among individuals with diabetes mellitus,with diabetic cardiomyopathy as the major diabetic cardiovascular complication.Hyperglycemia is a symptom that abnormally activates multiple downstream pathways and contributes to cardiac hypertrophy,fibrosis,apoptosis,and other pathophysiological changes.Although glycemic control has long been at the center of diabetes therapy,multicenter randomized clinical studies have revealed that intensive glycemic control fails to reduce heart failure-associated hospitalization and mortality in patients with diabetes.This finding indicates that hyperglycemic stress persists in the cardiovascular system of patients with diabetes even if blood glucose level is tightly controlled to the normal level.This process is now referred to as hyperglycemic memory(HGM)phenomenon.We briefly reviewed herein the current advances that have been achieved in research on the underlying mechanisms of HGM in diabetic cardiomyopathy.

关键词： diabetes diabetic cardiomyopathy hyperglycemic memory

MicroRNAs in cardiovascular diseases

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Medical Review 2022年第2期2卷 140-168页

作者： huaping li Jiabing Zhan Chen Chen Daowen Wang Division of Cardiology Department of Internal MedicineTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders WuhanChina.

Cardiovascular diseases(CVDs)are the leadingcauses of death and disability worldwide,despite thewide diversity of molecular targets identified and thedevelopment of therapeutic methods.MicroRNAs(miRNAs)are a class of small(about 22 nucleotides)non-codingRNAs(ncRNAs)that negatively regulate gene expressionat the post-transcriptional level in the cytoplasm and playcomplicated roles in different CVDs.While miRNA overexpression in one type of cell protects against heartdisease,it promotes cardiac dysfunction in another typeof cardiac cell.Moreover,recent studies have shown that,apart from cytosolic miRNAs,subcellular miRNAs suchas mitochondria-and nucleus-localized miRNAs aredysregulated in CVDs.However,the functional propertiesof cellular-and subcellular-localized miRNAs have notbeen well characterized.In this review article,by carefullyrevisiting animal-based miRNA studies in CVDs,we willaddress the regulation and functional properties ofmiRNAs in various CVDs.Specifically,the cell–cellcrosstalk and subcellular perspective of miRNAs arehighlighted.We will provide the background for attractivemolecular targets that might be useful in preventing theprogression of CVDs and heart failure(HF)as well asinsights for future studies.

关键词： apoptosis cardiovascular diseases fibrosis heart failure hypertrophy miRNAs subcellular organelle

A Kaposi’s sarcoma-associated herpes virus-encoded microRNA contributes to dilated cardiomyopathy

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Signal Transduction and Targeted Therapy 2023年第7期8卷 3443-3454页

作者： Yanru Zhao huaping li Hengzhi Du Zhongwei Yin Mengying He Jiahui Fan Xiang Nie Yang Sun Huiying Hou Beibei Dai Xudong Zhang Yuanyuan Cai Kunying Jin Nan Ding Zheng Wen Jiang Chang Chen Chen Dao Wen Wang Division of Cardiology Department of Internal MedicineTongji HospitalTongji Medical CollegeHuazhong University of Science and Technology430030 WuhanChina Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders 430030 WuhanChina Division of Cardiology Department of Internal MedicineHubei Provincial Renmin Hospital430030 WuhanChina Division of Cardiology Department of Internal MedicineThe First People’s Hospital of Anqing246004 AnqingChina Department of Epidemiology and Biostatistics Key Laboratory for Environment and HealthSchool of Public HealthTongji Medical CollegeHuazhong University of Science and Technology430030 WuhanChina

Dilated cardiomyopathy(DCM)is the leading cause of heart transplantation.By microRNA(miRNA)array,a Kaposi’s sarcoma-associated herpes virus(KSHV)-encoded miRNA,kshv-miR-K12-1-5p,was detected in patients with DCM.The KSHV DNA load and kshv-miR-K12-1-5p level in plasma from 696 patients with DCM were measured and these patients were followed-up.

关键词： Kaposi cardiomyopathy sarcoma

对比超声乳化术与小切口囊外摘除术治疗白内障的效果

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临床研究 2024年第1期32卷 53-56页

作者：李华萍河南省商丘市眼科医院眼科河南商丘476005

目的分析超声乳化术与小切口囊外摘除术治疗白内障的效果差异。方法回顾性分析商丘市眼科医院2018年1月至2022年12月接受治疗的白内障患者189人(189眼)的数据实施。依据患者所接受的手术方法差异实施分组,分为A组(接受超声乳化手术,n=93... 详细信息

目的分析超声乳化术与小切口囊外摘除术治疗白内障的效果差异。方法回顾性分析商丘市眼科医院2018年1月至2022年12月接受治疗的白内障患者189人(189眼)的数据实施。依据患者所接受的手术方法差异实施分组,分为A组(接受超声乳化手术,n=93)以及B组(接受小切口囊外摘除手术,n=96)。均选择术前(T_(1))、术后7 d(T_(2))、术后1个月(T_(3))、术后3个月(T_(4))共4个时间点的数据实施分析,对比两组患者治疗效果。对比两组患者不同时间点的视力情况、角膜内皮细胞数量、黄斑区厚度以及T_(4)时两组患者的黄斑水肿发生率,不同时间点手术源性角膜散光值,两组患者术后3个月内的并发症情况。结果T_(1)、T_(3)、T_(4)时间点,两组患者的裸眼视力、最佳矫正视力数据差异无统计学意义(P>0.05),T_(2)时间点,小切口囊外摘除手术组的裸眼视力、最佳矫正视力水平均优于于超声乳化术组,差异有统计学意义(P0.05),在T_(2)、T_(3)、T_(4)时间点,B组的角膜内皮细胞数量均高于A组,差异有统计学意义(P0.05),在T_(2)、T_(3)时间点,B组的黄斑区厚度均低于A组,差异有统计学意义(P0.05)。B组术后3个月的并发症发生率低于A组,差异有统计学意义(P<0.05)。结论针对白内障的患者,超声乳化术和小切口囊外摘除术均为有效的手术方法,两种方法相比,小切口囊外摘除术更利于患者术后短期的恢复以及围手术期并发症的降低。

关键词：超声乳化小切口囊外摘除白内障晶状体矫正视力

不同类型香蕉的细菌性鞘腐病病原分子鉴定及致病性分析

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华南农业大学学报 2024年第4期45卷 535-541页

作者：麦桂婉肖文超李云锋李华平饶雪琴广东省微生物信号与病害防治重点实验室/华南农业大学植物保护学院广东广州510642

[目的]香蕉Musa spp.是我国南方重要的经济作物,香蕉细菌性鞘腐病是近年来发现的一种细菌性病害,给香蕉生产带来严重影响。本研究旨在明确侵染不同类型香蕉的病原种类和致病性分化。[方法]对多种不同类型香蕉的细菌性鞘腐病病株进行分离... 详细信息

[目的]香蕉Musa spp.是我国南方重要的经济作物,香蕉细菌性鞘腐病是近年来发现的一种细菌性病害,给香蕉生产带来严重影响。本研究旨在明确侵染不同类型香蕉的病原种类和致病性分化。[方法]对多种不同类型香蕉的细菌性鞘腐病病株进行分离,并利用Dickeya属特异引物对这些病原进行PCR鉴定;通过分析16S rDNA核苷酸序列相似性、构建6个管家基因(fusA、gyrA、recA、gyrB、dnaJ和dnaX)的系统进化树并分析共线性关系进一步确定病原。采用离体和活体接种香蕉假茎及幼苗,对所分离病原进行致病性分析。[结果]从不同类型香蕉病株中共分离、获得15株菌株,PCR鉴定表明这些病原属于Dickeya spp.。16S rDNA核苷酸序列分析、基于6个管家基因的系统进化分析以及共线性分析的结果表明,所分离的菌株属于D. dadantii。致病性测定结果表明,这15株菌株致病性分为3类:1) XJ1、XJ8、XJ12和对照XJ5-1属于强致病力菌株;2) XJ2、XJ3、XJ4、XJ7和XJ11是较强致病力菌株;3) XJ5、XJ6、XJ9、XJ10和XJ13为中等致病力菌株。[结论]来源于不同类型香蕉的细菌性鞘腐病病原均为D. dadantii,不同菌株间存在明显的致病性分化,为进一步研究D.dadantii的致病机理以及香蕉细菌性鞘腐病的防控奠定了理论基础。

关键词：香蕉细菌性鞘腐病 Dickeya dadantii 致病性 16S rDNA

Nuclear miR-665 aggravates heart failure via suppressing phosphatase and tensin homolog transcription

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Science China(life Sciences) 2020年第5期63卷 724-736页

作者： Jiahui Fan Xudong Zhang Xiang Nie huaping li Shuai Yuan Beibei Dai Jiabing Zhan Zheng Wen Jiangang Jiang Chen Chen Daowen Wang Division of Cardiology Department of Internal MedicineTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders Wuhan 430030China

Although numerous miRNAs have been discovered,their functions in the different subcellular organelles have remained obscure.In this study,we found that miR-665 was enriched in the nucleus of cardiomyocytes,and then investigated the underlying role of nuclear miR-665 in heart failure.RNA fluorescence in situ hybridization assays in human heart tissue sections and primary cardiomyocytes showed that miR-665 was localized in the nucleus of cardiomyocytes.Increased expression of nuclear miR-665 was observed not only in the cardiomyocytes isolated from the heart of mice treated in vivo by transverse aortic constriction(TAC),but also in phenylephrine(PE)-treated cultured cardiomyocytes in vitro.To further explore the role of miR-665 in heart failure,a type 9 recombinant adeno-associated virus(rAAV)system was employed to manipulate the expression of miR-665 in mice.Overexpression of miR-665 aggravated TAC-induced cardiac dysfunction,while down-expression of miR-665 showed opposite effects.Bioinformatic prediction and biological validation confirmed that the PTEN(phosphatase and tensin homolog)gene was one of the targets of miR-665 in the nucleus.Furthermore,restoring PTEN expression significantly eliminated the destructive effects of miR-665 over-expression in TAC-induced cardiac dysfunction.Our data showed that nuclear miR-665 aggravates heart failure via inhibiting PTEN expression,which provided a therapeutic approach for heart failure.

关键词： nucleus miR-665 heart failure phosphatase and tensin homolog

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妊娠期高血糖与胎盘滋养细胞衰老的研究进展

中国优生与遗传杂志 2024年第1期32卷 208-213页

作者：郑琳李华萍上海交通大学医学院附属第六人民医院妇产科上海200233 上海市第六人民医院金山分院妇产科上海201599

妊娠期高血糖包括孕前糖尿病、糖尿病前期和妊娠糖尿病,易导致多种不良妊娠结局的发生,然而高血糖状态及影响母子健康的分子机制尚不清晰。研究表明细胞衰老是在多种驱动因素作用下出现不可逆的细胞生长停滞现象,这种现象与机体疾病密... 详细信息

妊娠期高血糖包括孕前糖尿病、糖尿病前期和妊娠糖尿病,易导致多种不良妊娠结局的发生,然而高血糖状态及影响母子健康的分子机制尚不清晰。研究表明细胞衰老是在多种驱动因素作用下出现不可逆的细胞生长停滞现象,这种现象与机体疾病密切相关,不仅在损伤修复和肿瘤抑制等方面发挥作用,而且与糖尿病的发生发展相关。近年多项研究发现,高血糖可能通过多种途径诱导滋养细胞异常衰老,不同糖代谢状态和胎盘滋养细胞衰老互相影响,可能决定着妊娠糖尿病的发生发展和母胎结局,据此,本文主要对正常妊娠与胎盘滋养细胞衰老、妊娠期高血糖与胎盘滋养细胞异常衰老、胎盘滋养细胞衰老与不良妊娠结局等方面的研究进展进行综述,以期从新的视角认识妊娠期高血糖导致不良妊娠结局的分子机制。

关键词：妊娠期高血糖细胞衰老滋养细胞妊娠结局

The double face of miR-320:cardiomyocytes-derived miR-320 deteriorated while fibroblasts-derived miR-320 protected against heart failure induced by transverse aortic constriction

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Signal Transduction and Targeted Therapy 2021年第3期6卷 950-961页

作者： Xudong Zhang Shuai Yuan huaping li Jiabing Zhan Feng Wang Jiahui Fan Xiang Nie Yan Wang Zheng Wen Yanghui Chen Chen Chen Dao Wen Wang Division of Cardiology Tongji HospitalTongji Medical College and Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiologic DisordersHuazhong University of Science and TechnologyWuhan 430030China

MicroRNAs(miRNAs)are aberrantly expressed in the pathophysiologic process of heart failure(HF).However,the functions of a certain miRNA in different cardiac cell types during HF are scarcely reported,which might be covered by the globe effects of it on the heart.In the current study,Langendorff system was applied to isolate card io myocytes(CMs)and cardiac fibroblasts(CFs)from transverse aortic constriction(TAC)-induced mice.Slight increase of miR-320 expression was observed in the whole heart tissue of TAC mice.Interestingly,miR-320 was significantly elevated in CMs but decreased in CFs from TAC mice at different time points.Then,recombinant adeno-associated virus 9 with cell-type-specific promoters were used to manipulate miR-320 expressions in vivo.Both in vitro and in vivo experiments showed the miR-320 overexpression in CMs exacerbated cardiac dysfunction,whereas overexpression of miR-320 in CFs alleviated cardiac fibrosis and hypertrophy.Mechanically,downstream signaling pathway analyses revealed that miR-320 might induce various effects via targeting PLEKHM3 and IFITM1 in CMs and CFs,respectively.Moreover,miR-320 mediated effects could be abolished by PLEKHM3 re-expression in CMs or IFITM1 re-expression in CFs.Interestingly,miR-320 treated CFs were able to indirectly affect CMs function,but not vice versa.Meanwhile,upstream signaling pathway analyses showed that miR-320 expression and decay rate were rigorously manipulated by Ago2,which was regulated by a cluster of cell-type-specific TFs distinctively expressed in CMs and CFs,respectively.Together,we demonstrated that miR-320 functioned differently in various cell types of the heart during the progression of HF.

关键词： miR elevated transverse