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Emerging role of lncRNAs as mechanical signaling molecules in mechanotransduction and their association with Hippo-YAP signaling:a review

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第4期25卷 280-292页

作者： Siyi LIN Xinyu HE Ying WANG Yu CHEN Aifu LIN College of Medicine Zhejiang UniversityHangzhou 310058China College of Life Sciences Zhejiang UniversityHangzhou 310058China Cancer Center Zhejiang UniversityHangzhou 310058China Key Laboratory for Cell and Gene Engineering of Zhejiang Province Hangzhou 310058China International School of Medicine International Institutes of Medicinethe Fourth Affiliated Hospital of Zhejiang University School of MedicineYiwu 322000China Key Laboratory of Cancer Prevention and Intervention China National Ministry of EducationHangzhou 310058China future Health Laboratory Innovation Center of Yangtze River DeltaZhejiang UniversityJiaxing 314100China

Cells within tissues are subject to various mechanical forces,including hydrostatic pressure,shear stress,compression,and tension.These mechanical stimuli can be converted into biochemical signals through mechanoreceptors or cytoskeleton-dependent response processes,shaping the microenvironment and maintaining cellular physiological balance.Several studies have demonstrated the roles of Yes-associated protein(YAP)and its homolog transcriptional coactivator with PDZ-binding motif(TAZ)as mechanotransducers,exerting dynamic influence on cellular phenotypes including differentiation and disease pathogenesis.This regulatory function entails the involvement of the cytoskeleton,nucleoskeleton,integrin,focal adhesions(fAs),and the integration of multiple signaling pathways,including extracellular signal-regulated kinase(ERK),wingless/integrated(WNT),and Hippo signaling.furthermore,emerging evidence substantiates the implication of long non-coding RNAs(lncRNAs)as mechanosensitive molecules in cellular mechanotransduction.In this review,we discuss the mechanisms through which YAP/TAZ and lncRNAs serve as effectors in responding to mechanical stimuli.Additionally,we summarize and elaborate on the crucial signal molecules involved in mechanotransduction.

关键词： YAP/TAZ Long non-coding RNA(lncRNA) Mechanotransduction f-actin

CXCR5 Regulates Neuronal Polarity Development and Migration in the Embryonic Stage via f‑actin Homeostasis and Results in Epilepsy‑Related Behavior

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Neuroscience Bulletin 2023年第11期39卷 1605-1622页

作者： Zhijuan Zhang Hui Zhang Ana Antonic‑Baker Patrick Kwan Yin Yan Yuanlin Ma Department of Neurology Chongqing Key Laboratory of NeurologyThe First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Chongqing Emergency Medical Center The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Department of Neuroscience Central Clinical SchoolMonash UniversityMelbourneAustralia

Epilepsy is a common,chronic neurological disorder that has been associated with impaired neurodevelopment and immunity.The chemokine receptor CXCR5 is involved in seizures via an unknown mechanism.Here,we first determined the expression pattern and distribution of the CXCR5 gene in the mouse brain during different stages of development and the brain tissue of patients with epilepsy.Subsequently,we found that the knockdown of CXCR5 increased the susceptibility of mice to pentylenetetrazol-and kainic acid-induced seizures,whereas CXCR5 overexpression had the opposite effect.CXCR5 knockdown in mouse embryos via viral vector electrotransfer negatively influenced the motility and multipolar-to-bipolar transition of migratory neurons.Using a human-derived induced an in vitro multipotential stem cell neurodevelopmental model,we determined that CXCR5 regulates neuronal migration and polarization by stabilizing the actin cytoskeleton during various stages of neurodevelopment.Electrophysiological experiments demonstrated that the knockdown of CXCR5 induced neuronal hyperexcitability,resulting in an increased number of seizures.finally,our results suggested that CXCR5 deficiency triggers seizure-related electrical activity through a previously unknown mechanism,namely,the disruption of neuronal polarity.

关键词： Epilepsy CXCR5 Embryonic neurogenesis Pluripotent stem cells Intrauterine electroporation f-actin Neuronal polarity Neuronal migration

Arabidopsis ROP1 and ROP6 Influence Germination Time, Root Morphology, the formation of f-actin Bundles, and Symbiotic fungal Interactions

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Molecular Plant 2013年第3期6卷 872-886页

作者： Yvonne Venus Institut f~r ALLgemeine Botanik und Pflanzenphysiologie Friedrich-Schiller-Universit ~t Jena Dornburger Strafe 159 D-07743 Jena Germany

The RHO-related GTPases ROP1 and ROP6 and the ROPl-interacting protein RIC4 in Arabidopsis are involved in various processes of f-actin dynamics, cell growth, and plant/microbe interactions. The knockout ropl and ropl rop6 seeds germinate earlier and are impaired in root hair development. Also root hair branching is strongly affected by manipulation of the RHO-related GTPase （ROP） levels. furthermore, in the double knockout line ropl rop6, no actin bundle formation can be detected. We demonstrate that these proteins are required for establishing a mutualistic interaction between the root-colonizing endophytic fungus Piriformospora indica and Arabidopsis. The fungus promotes growth of wild-type plants, ropl, rop6, ropl rop6, ric4, 35S：：ROP1, and 35S：：ROP6 seedlings are impaired in the response to the fungus. Since the different root architectures have no effect on root colonization, the impaired response to P. indica should be caused by ROP-mediated events in the root cells. In wild-type roots, P. indica stimulates the formation of f-actin bundles and this does not occur in the ropl rop6 knockout line. furthermore, the fungus stimulates the expression of the calmodulin-binding protein gene Cbp60g, and this response is severely reduced in the rop mutants. We propose that ROP1 and ROP6 are required for f-actin bundle formation in the roots, which is required for P. indica-mediated growth promotion in Arabidopsis.

关键词： Cbp6Og cytoskeleton f-actin GTPases Piriformospora indica ROP.

DnaJA4 is involved in responses to hyperthermia by regulating the expression of f-actin in HaCaT cells

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Chinese Medical Journal 2021年第4期134卷 456-462页

作者： Rui-Jiao Liu Xue-Li Niu Jin-Ping Yuan Hong-Duo Chen Xing-Hua Gao Rui-Qun Qi Department of Dermatology The First Hospital of China Medical UniversityShenyangLiaoning 110001China National Health Commission Key Laboratory of Immunodermatology(China Medical University) ShenyangLiaoning 110001China Key Laboratory of Immunodermatology(China Medical University) Ministry of EducationShenyangLiaoning 110001China National and Local Joint Engineering Research Center of Immunodermatological Theranostics ShenyangLiaoning 110001China.

Background:Hyperthermia in combination with DnaJA4-knockout(KO)obviously affects the anti-viral immunity of HaCaT cells.The mechanisms of this process are not yet fully explored.However,it is known that DnaJA4 interacts with actin cytoskeleton after hyperthermia.Our aim was to investigate the effects of DnaJA4 on f-actin in HaCaT cells following hyperthermia.Methods:Wild-type(WT)and DnaJA4-KO HaCaT cells were isolated at either 37°C(unheated)or 44°C(hyperthermia)for 30 min followed by testing under conditions of 37°C and assessing at 6,12,and 24 h after hyperthermia.The cytoskeleton was observed with immunofluorescence.flow cytometry and Western blotting were used to detect the expression of f-actin and relevant pathway protein.Results:DnaJA4-KO and hyperthermia changed the cytoskeleton morphology of HaCaT cells.f-actin expression levels were elevated in DnaJA4-KO cells compared with WT cells(6364.33±989.10 vs.4272.67±918.50,Pf-actin expression levels of both WT and DnaJA4-KO cells showed a tendency to decrease followed by an obvious recovery after hyperthermia(WT cells:unheated vs.6 h after hyperthermia or 24 h after hyperthermia:0.34±0.02 vs.0.24±0.01,0.31±0.01,Pfter hyperthermia or 24 h after hyperthermia:0.44±0.01 vs.0.30±0.01,0.51±0.02,Pfactors of f-actin,a similar profile in rho-associated serine/threonine kinase 1(ROCK 1)and RhoA expressions was observed after hyperthermia.While E-cadherin expression was decreased in response to hyperthermia,it was increased in DnaJA4-KO cells compared with WT cells.Conclusions:Hyperthermia affects the expression levels of f-actin in HaCaT cells.DnaJA4 knockout increases the expression of f-actin in HaCaT cells after hyperthermia.DnaJA4 regulates the expressions of f-actin and the related pathway proteins in response to hyperther

关键词： Hyperthermia DnaJA4 f-actin HaCaT

Hsp90 inhibition induces destabilization of actin cytoskeleton in tumor cells:functional significance of Hsp90 interaction with f-actin

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Asian Pacific Journal of Tropical Medicine 2010年第9期3卷 715-722页

作者： Vishal Chaturvedi Amere Subbarao Sreedhar Centre for Cellular and Molecular Biology Uppal RoadHyderabad 500 007India

Objective:To examine the role of heat shock protein 90(Hsp90) in the maintenance of actin cytoskeleton in human neuroblastoma tumor cells.Methods:Co-precipitation experiments were performed to examine Hsp90 interaction with actin.Hsp90 and actin interactions were evaluated by protein refolding and acto-myosin motility assays.17-(AUylamino)-17- demethoxygeldanamycin(17AAG) induced actin-cytoskeleton re-organization was examined by laser scanning confocal microcopy.Results:It was shown that inhibition of Hsp90 by 17AAC accelerates detergent induced cell lysis of neuroblastoma tumor cells through destabilization of actin cytoskeleton.The in vitro co-precipitation experiments showed that functional but not mutant Hsp90 binds with f-actin.Among biochemical modifications,phopshorylation and oligomerization enhanced Hsp90 binding with f-actin.f-actin binding to Hsp90 interfered with Hsp90 chaperone activity in protein refolding assays,and Hsp90 binding to f-actin interfered with actin motility on myosin coated flow cell.In the combination treatment,17AAG irreversibly augmented the effect of cytochalasin D,an inhibitor of actin polymerization.Conclusions:It can be concluded that Hsp90 binds to f-actin in tumor cells and maintains the cellular integrity. The results display a novel element of Hsp90 inhibition in destabilizing the actin cytoskeleton of tumor cells,therefore suggest that 17AAG combination with cytoskeletal disruptor may be effective in combating cancer.

关键词： Hsp90 f-actin Cytoskeleton 17AAG Tumor cells Combination treatment

Effect of hepatic ischemia-reperfusion on bile canalicular f-actin microfilaments in rats

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Journal of Nanjing Medical University 2009年第2期23卷 137-142页

作者： Yiming Li Hua Li Jidong Liu Hong Ji Department of General Surgery the Second Affiliated Hospital of Xi' an Jiaotong University Xi' an 710004 China

Objective：To investigate the effect of hepatic ischemia-reperfusion（I/R） on bile canalicular f-actin microfilaments in rats. Methods： A rat model of hepatic ischemia-reperfusion was employed and the ischemia time was 35 min. The activity of serum alanine aminotransferase （ALT）, aspartate aminotransferase（AST）, γ-glutamyl transferase（GGT） and the level of total bilirubin（TBIL） were measured. Changes in the bile canaliculi were observed by transmission electron microscope. The modification of f-actin microfilaments was quantified by using fITC-Phalloidin and analyzed by confocal laser scanning microscopy imaging. Results：Modifications of f-actin staining were consistent with the observations made by transmission electron microscopy. The staining of f-actin was normal in hepatocytes before reperfusion but decreased significantly after reperfusion, and there was a marked loss of canalicular microvilli after reperfusion, which coincided with abnormal serum GGT and TBIL levels. Conclusion：Reperfusion, not short-term ischemia, induced a disruption of f-actin microfilaments and a loss of microvilli. These modifications could lead to the impaired bile secretion by damaging canalicular contraction, and could be the main mechanisms of cholestasis after hepatic ischemia-reperfusion in rats.

关键词： ischemia-reperfusion cholestasis f-actin

ECT2/SERPINE1/f-actin促进胶质瘤侵袭迁移能力机制的研究

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ECT2/SERPINE1/F-actin促进胶质瘤侵袭迁移能力机制的研究

作者：陈光樑苏州大学

学位级别：硕士

研究背景:胶质瘤是成年人常见的原发性脑恶性肿瘤之一,其中恶性程度最高的是胶质母细胞瘤(Glioblastoma,GBM),对人类健康危害极大,预后不良。GBM患者预后差很大程度上是由于其侵袭能力强,瘤细胞异质性大以及手术无法实现肿瘤完全切除等... 详细信息

研究背景:胶质瘤是成年人常见的原发性脑恶性肿瘤之一,其中恶性程度最高的是胶质母细胞瘤(Glioblastoma,GBM),对人类健康危害极大,预后不良。GBM患者预后差很大程度上是由于其侵袭能力强,瘤细胞异质性大以及手术无法实现肿瘤完全切除等特点,即使随后同步放疗及替莫唑胺化疗,仍无法控制肿瘤的复发。在分子靶向治疗角度深入研究胶质瘤的发生与发展,并从中寻找更为有效特异的治疗方法仍是当今胶质母细胞瘤研究的热点。上皮细胞转化序列2作为一种鸟嘌呤核苷酸转换因子可促进Rho蛋白的鸟嘌呤核苷酸转换,使其激活进而介导下游通路,调控细胞诸多生命活动。近期研究表明,ECT2作为一种原癌基因在包括胶质瘤在内的多种人类恶性肿瘤中过度表达,同时ECT2的表达情况与肿瘤患者的不良生存预后密切相关,表明ECT2在恶性肿瘤的发生发展中发挥着重要作用,但是其在胶质瘤中的具体调控机制仍有待进一步探究。研究目的:本课题旨在探讨胶质瘤中ECT2的表达情况及其对胶质瘤患者生存预后的影响,研究靶向敲低ECT2基因后对胶质母细胞瘤细胞表型的影响,并通过生物信息学及蛋白组学分析找寻其调控的分子机制下游,为分子靶向ECT2治疗胶质瘤提供进一步的理论科学依据。研究方法:1、通过TCGA和CGGA数据库收集肿瘤相关的生物信息,研究ECT2基因在胶质瘤组织中的表达及其与患者生存预后的相关性。并通过免疫印迹技术与免疫组化技术检测ECT2基因在非瘤脑组织与脑胶质瘤组织中的表达情况。2、利用干扰RNA转染技术针对人脑胶质母细胞瘤细胞的ECT2基因进行敲低,其次采用免疫印迹、免疫荧光技术检测敲低效果。进一步通过CCK-8、细胞划痕、Transwell等实验探究ECT2敲低对胶质瘤细胞增殖、侵袭、迁移能力的影响。3、通过TMT标记定量蛋白组实验分析检测ECT2基因表达敲低后胶质母细胞瘤细胞在蛋白水平差异表达情况。利用常见的多个数据库对鉴定的蛋白进行功能注释分析。对筛选得到的差异蛋白进行GO、KEGG和蛋白互作网络分析,同时进行相关性分析、表达模式聚类热图和火山图等数据分析。依据蛋白组学分析结果及研究的相关性,确定位于ECT2基因调控下游的关键蛋白。4、通过免疫共沉淀(Co-Immunoprecipition,Co-IP)实验、免疫荧光共定位实验及数据库生物信息学分析结果确定ECT2与SERPINE1在细胞内存在蛋白互作捆绑作用及胞内功能的亚定位。通过蛋白质免疫印迹、免疫荧光的方法检测侵袭迁移相关蛋白CDH1、CDH2、MMP2的变化。通过荧光明胶基质降解实验检测ECT2敲低后对胶质母细胞瘤f-actin蛋白含量表达及对细胞外基质降解能力的影响。5、构建裸鼠颅内原位肿瘤模型,设计体内实验,通过荧光素酶活体成像技术动态检测颅内裸鼠成瘤进展,收集裸鼠生存统计数据,分析ECT2表达敲低后胶质瘤颅内肿瘤模型对裸鼠造成的生存期差异。通过HE染色法及免疫组化染色检测目的蛋白及侵袭迁移相关蛋白的表达情况,用于评估ECT2基因对胶质瘤细胞体内成瘤性的影响及靶向ECT2的治疗效果。研究结果:1、通过对临床来源的脑组织标本行切片免疫组化染色及蛋白质免疫分析可见,脑胶质瘤组织中ECT2表达明显高于非瘤脑组织,且随着肿瘤恶性度的提高,ECT2的表达量也随之升高(pfC≥1.5且p<0.05为标准筛选差异蛋白,共得到84个上调蛋白与161个下调蛋白,并对上调差异最明显的20个蛋白与下调最明显的20个蛋白行聚类热图分析。对差异表达蛋白行GO分析、KEGG分析可见其功能主要富集与

关键词：胶质瘤 ECT2 SERPINE1 f-actin 细胞侵袭与迁移

Peripheral nerve fibroblasts secrete neurotrophic factors to promote axon growth of motoneurons

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Neural Regeneration Research 2022年第8期17卷 1833-1840页

作者： Qian-Ru He Meng Cong fan-Hui Yu Yu-Hua Ji Shu Yu Hai-Yan Shi fei Ding Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education Co-Innovation Center of NeuroregenerationJiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury RepairNantong UniversityNantongJiangsu ProvinceChina

Peripheral nerve fibroblasts play a critical role in nerve development and regeneration.Our previous study found that peripheral nerve fibroblasts have different sensory and motor phenotypes.fibroblasts of different phenotypes can guide the migration of Schwann cells to the same sensory or motor phenotype.In this study,we analyzed the different effects of peripheral nerve-derived fibroblasts and cardiac fibroblasts on motoneurons.Compared with cardiac fibroblasts,peripheral nerve fibroblasts greatly promoted motoneuron neurite outgrowth.Transcriptome analysis results identified 491 genes that were differentially expressed in peripheral nerve fibroblasts and cardiac fibroblasts.Among these,130 were significantly upregulated in peripheral nerve fibroblasts compared with cardiac fibroblasts.These genes may be involved in axon guidance and neuron projection.Three days after sciatic nerve transection in rats,peripheral nerve fibroblasts accumulated in the proximal and distal nerve stumps,and most expressed brain-derived neurotrophic factor.In vitro,brain-derived neurotrophic factor secreted from peripheral nerve fibroblasts increased the expression ofβ-actin and f-actin through the extracellular regulated protein kinase and serine/threonine kinase pathways,and enhanced motoneuron neurite outgrowth.These findings suggest that peripheral nerve fibroblasts and cardiac fibroblasts exhibit different patterns of gene expression.Peripheral nerve fibroblasts can promote motoneuron neurite outgrowth.

关键词： brain-derived neurotrophic factor differential gene expression f-actin fibroblasts motoneurons mRNA sequencing neurite outgrowth peripheral nervous system β-actin

ISKNV介导Rac1-PAK1-LIMK-Cofilin信号通路调控f-actin重排促进自身复制增殖

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ISKNV介导Rac1-PAK1-LIMK-Cofilin信号通路调控F-actin重排促进自...

作者：谭有燕上海海洋大学

学位级别：硕士

传染性脾肾坏死病毒(Infectious spleen and kidney necrosis virus,ISKNV)可感染多种鱼类,是造成鳜发病的主要病原之一,严重危害鳜养殖业的健康发展。微丝(f-actin)是细胞骨架的重要组成成分,在病毒吸附、入侵及组装和释放过程中发挥... 详细信息

传染性脾肾坏死病毒(Infectious spleen and kidney necrosis virus,ISKNV)可感染多种鱼类,是造成鳜发病的主要病原之一,严重危害鳜养殖业的健康发展。微丝(f-actin)是细胞骨架的重要组成成分,在病毒吸附、入侵及组装和释放过程中发挥重要作用。有研究发现f-actin在ISKNV感染晚期具有重要作用。那么f-actin与ISKNV复制增殖存在什么关系?参与调控f-actin的信号通路有哪些?它们又怎样调控ISKNV复制增殖?带着上述问题,我们开展如下研究:1.f-actin与ISKNV复制增殖的关系ISKNV感染鳜脑细胞系(Chinese perch brain cell line,CPB),RT-q PCR检测ISKNV不同时间点拷贝数变化,结果显示ISKNV感染72 h是病毒复制的高峰期。在此时间段对细胞f-actin间接免疫荧光染色,与对照细胞相比,ISKNV感染后的f-actin聚集在病毒的病变位置,说明ISKNV的复制增殖会导致f-actin发生重排。利用f-actin抑制剂Cytochalasin D和Cucurbitacin E预处理细胞,抑制f-actin重排,RT-q PCR、Western blot和TCID检测其对ISKNV复制增殖的影响。结果显示抑制f-actin重排后,ISKNV的病变细胞、病毒基因组拷贝数和病毒蛋白表达呈剂量依赖性下调,病毒滴度降低。上述结果说明,ISKNV诱导f-actin重排促进病毒的复制增殖。2.Rho A-Rock 1和Rac1-PAK1信号通路与ISKNV复制增殖的关系f-actin是高度动态变化的结构,由Rho GTPases家族成员通过传递膜受体信号调控。Rho A及Rac1是Rho-GTPase家族主要成员。为了探究Rho A和Rac1及其下游信号通路是否参与ISKNV的感染,RT-q PCR和Western blot对病毒感染72 h后细胞内的Rho A、Rock 1、Rac1、PAK1进行测定。RT-q PCR发现病毒感染72 h的Rho A、Rock 1、Rac1及PAK1 m RNA上调;Western blot结果显示,病毒感染72 h的Rho A、Rock 1、Rac1及PAK1蛋白表达显著上调,PAK1的磷酸化显著上调,说明Rho A-Rock 1和Rac1-PAK1信号通路均参与了ISKNV复制增殖。为了进一步阐释Rho A-Rock 1和Rac1-PAK1通路与ISKNV复制增殖的关系,利用抑制剂CCG-1423、Thiazovivin、Ehop-016和IPA-3分别抑制Rho A-Rock 1和Rac1-PAK1通路。RT-q PCR发现抑制Rho A-Rock 1通路后ISKNV基因组D NA拷贝数降低2.4倍,ISKNV引起的细胞病变减少2.3倍,以上结果说明抑制R ho A-Rock 1通路后抑制ISKNV复制增殖。抑制Rac1-PAK1通路后,ISKNV基因组DNA拷贝数降低4.3倍,ISKNV引起的细胞病变减少5.8倍,ISKNV-MCP蛋白表达下调3.4倍,说明抑制Rac1-PAK1通路显著抑制ISKNV的复制增殖。对抑制剂Ehop-016和IPA-3处理后的细胞进行荧光染色,发现抑制剂抑制病毒诱发的f-actin重排,说明在ISKNV复制增殖中,Rac1-PAK1信号通路调控f-actin重排。综上,抑制Rho A-Rock 1和Rac1-PAK1通路均可抑制ISKNV复制增殖,但Rac1-PAK1通路对ISKNV的复制增殖影响更显著,因此本实验后续主要以Rac1-PAK1为研究对象。3.LIMK-Cofilin信号通路与ISKNV复制增殖的关系LIMK是丝氨酸/苏氨酸蛋白激酶家族中的一员,是PAK1下游激酶。RT-q PC R和Western blot检测LIMK在ISKNV复制增殖过程中的激活情况及对病毒复制增殖的影响。结果显示ISKNV感染细胞72 h后,细胞LIMK m RNA表达、LIM K蛋白表达及磷酸化的LIMK蛋白表达均显著上调,LIMK活性明显上调,这与P AK1的变化趋势相一致。si RNA敲降细胞内源性LIMK基因后,RT-q PCR和We stern blot检测ISKNV感染量的变化,结果显示ISKNV的复制增殖被明显抑制,表明ISKNV介导LIMK调控病毒复制增殖。LIMK可调控其下游激酶Cofilin使其磷酸化而失活。利用RT-q PCR和Weste rn blot检测ISKNV感染后Cofilin激活情况,结果显示ISKNV感染细胞72 h后,胞内Cofilin m RNA表达显著上调,Cofilin蛋白表达显著上调,磷酸化的Cofilin蛋白表达显著下调,Cofilin活性显著升高。采用si RNA敲降CPB细胞内Cofilin后感染ISKNV,RT

关键词：传染性脾肾坏死病毒 f-actin Rac1-PAK1-LIMK-Cofilin信号通路调控复制增殖