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H3K36 methyltransferase NSD1 regulates chondrocyte differentiation for skeletal development and fracture repair

Bone Research 2021年第3期9卷 349-359页

作者： Rui Shao Zhong Zhang Zhan Xu Huiling Ouyang Lijun Wang Hongwei Ouyang Matthew Greenblatt Xi Chen Weiguo Zou Shanghai Institute of Microsurgery on Extremities and Department of Orthopedic SurgeryShanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghaiChina State Key Laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell BiologyCAS Center for Excellence in Molecular Cell SciencesChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghaiChina Dr.Li Dak Sum&Yip Yio Chin Center for Stem Cell and Regenerative Medicine Zhejiang University-University of Edinburgh InstituteZhejiang UniversityHangzhouZhejiangChina China Orthopedic Regenerative Medicine Group HangzhouZhejiangChina Department of Pathology and Laboratory Medicine Weill Cornell MedicineNew YorkNYUSA Department of Molecular and Cellular Biology Lester and Sue Smith Breast CenterDan L.Duncan Cancer CenterBaylor College of MedicineHoustonTXUSA

Chondrocyte differentiation is a critical process for endochondral ossification,which is responsible for long bone development and fracture *** progress has been made in understanding the transcriptional control of chondrocyte differentiation;however,epigenetic regulation of chondrocyte differentiation remains to be further ***1 is a H3K36(histone H3 at lysine 36)***,we showed that mice with Nsd1 deficiency in Prx1+mesenchymal progenitors but not in Col2+chondrocytes showed impaired skeletal growth and fracture healing accompanied by decreased chondrogenic *** combined RNA sequencing(RNA-seq)and chromatin immunoprecipitation sequencing(ChIP-seq)analysis,we identified sex determining region Y box 9(Sox9),the key transcription factor of chondrogenic differentiation,as a functional target gene of ***,NSD1 regulates Sox9 expression by modulating H3K36me1 and H3K36me2 levels in the Sox9 promoter region,constituting a novel epigenetic regulatory mechanism of ***,we found that NSD1 can directly activate the expression of hypoxia-inducible factor 1α(HIF1α),which plays a vital role in chondrogenic differentiation through its regulation of Sox9 ***,the results of our study reveal crucial roles of NSD1 in regulating chondrogenic differentiation,skeletal growth,and fracture repair and expand our understanding of the function of epigenetic regulation in chondrogenesis and skeletal biology.

关键词： skeletal impaired healing

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EGFR TKIs impair lysosome-dependent degradation of SQSTM1 to compromise the effectiveness in lung cancer

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Signal Transduction and Targeted Therapy 2019年第1期4卷 482-492页

作者： Lixian Yang Shilong Ying Shiman Hu Xiangtong Zhao Muchun Li Miaoqin Chen Yiran Zhu Ping Song Liyuan Zhu Tingting Jiang Huimin An Neelum Aziz Yousafzai Wenxia Xu Zhiguo Zhang Xian Wang Lifeng Feng Hongchuan Jin Laboratory of Cancer Biology Key Lab of Biotherapy in ZhejiangSir Run Run Shaw HospitalMedical School of Zhejiang UniversityHangzhouChina Department of Medical Oncology Key Lab of Biotherapy in ZhejiangSir Run Run Shaw HospitalMedical School of Zhejiang UniversityHangzhouChina Department of Pathology Sir Run Run Shaw HospitalMedical School of Zhejiang UniversityHangzhouChina Key Laboratory of Biomass Chemical Engineering of Ministry of Education College of Chemical and Biological EngineeringZhejiang UniversityHangzhouChina

Tyrosine kinase inhibitors for epidermal growth factor receptor(EGFR TKIs)greatly improved clinical outcomes of patients with non-small cell lung cancer(NSCLC).Unfortunately,primary and acquired resistance limits their clinical *** overcome such resistance,new generations of EGFR TKIs have been developed by targeting newly identified mutations in ***,much less effort has been put into alternative strategies,such as targeting the intrinsic protective responses to EGFR *** this study,we found that EGFR TKIs,including gefitinib and AZD9291,impaired lysosome-dependent degradation of SQSTM1,thus compromising their anti-cancer *** accumulating in the lysosome lumen,gefitinib and AZD9291 attenuated lysosomal acidification and impaired autolysosomal degradation of SQSTM1 owing to their intrinsic *** a result,SQSTM1 protein was stabilized in response to gefitinib and AZD9291 treatment and conferred EGFR TKI *** SQSTM1 significantly increased the sensitivity of NSCLC cells to gefitinib and AZD9291 both in vitro and in ***,a chemically modified gefitinib analog lacking alkalinity displayed stronger inhibitory effects on NSCLC ***,targeting accumulated SQSTM1 or chemically modified EGFR TKIs may represent new strategies to increase the effectiveness of EGFR targeted therapy.

关键词： impaired protective alkali

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Genetic profile of Chinese patients with Charcot-Marie-Tooth disease

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Chinese Medical Journal 2020年第21期133卷 2633-2634页

作者： Zhi-Yuan Ouyang You Chen Da-Qiang Qin Zhi-Dong Cen Xiao-Sheng Zheng Fei Xie Si Chen Hao-Tian Wang De-Hao Yang Xin-Hui Chen Le-Bo Wang Bao-Rong Zhang Wei Luo Department of Neurology The Second Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310009China Cancer Institute Key Laboratory of Cancer Prevention and InterventionChina National Ministry of EducationThe Second Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310009China Department of Neurology Affiliated Hospital of Jiangsu UniversityZhenjiangJiangsu 212001China Department of Intensive Care Unit Zhejiang HospitalHangzhouZhejiang 310030China Department of Neurology Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhouZhejiang 310016China Chu Kochen Honors College Zhejiang UniversityHangzhouZhejiang 310058China

To the Editor:Charcot-Marie-Tooth disease(CMT)encompasses a genetically heterogeneous group of inherited neuropathies,characterized by progressive distal muscle weakness and atrophy,sensory deficits,impaired tendon reflexes,and foot deformities.[1]To date,more than 80 causative genes have been identified in CMT patients,associated with either autosomal dominant or recessive inheritance,or X-linked *** traditional classification of CMT was based on peripheral neuropathy type,as determined by nerve conduction *** more causative genes were identified and the overlap of neuropathy phenotypes became apparent,the traditional classification system proved unwieldy and ***,CMT needs to be distinguished from several entities including systemic disorders with neuropathy and other types of hereditary *** clinical practice,overlap of phenotypes can present a major challenge in reaching the correct *** study aimed to investigate the genetic profile in a cohort of Chinese CMT patients and evaluate the role of genetic testing in the diagnosis and subtyping of CMT.

关键词： Marie patients impaired

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Short-chain fatty acids in the context of Parkinson’s disease

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Neural Regeneration Research 2021年第10期16卷 2015-2016页

作者： Judith Metzdorf Lars Tonges Department of Neurology St.Josef-HospitalRuhr-University BochumBochumGermany

Research on neurodegenerative diseases such as Alzheimer’s disease,Parkinson´s disease(PD),Huntington’s disease or amyotrophic lateral sclerosis is becoming increasingly important in our *** to the ageing of the population,the prevalence of these diseases continue to rise worldwide,and causal cures are not yet available(Erkkinen et al.,2018).This Perspective focusses on PD,a movement disorder of the central nervous system with an estimated prevalence between 65 and 1250/100,000 in Europe,affecting about 1 percent of the population older than 60 *** clinical symptoms include motor symptoms like bradykinesia,tremor or rigidity which are associated with loss of dopaminergic neurons in the substantia nigra and their innervating axonal fibers to the *** non-motor symptoms may consist in depression,hyposmia,cognitive decline or constipation due to impaired motility of the gastrointestinal tract.

关键词： Huntington impaired diseases

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Gibberellin repression of axillary bud formation in Arabidopsis by modulation of DELLA-SPL9 complex activity

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Journal of Integrative Plant Biology 2020年第4期62卷 421-432页

作者： Qi-Qi Zhang Jia-Gang Wang Ling-Yan Wang Jun-Fang Wang Qun Wang Ping Yu Ming-Yi Bai Min Fan Key Laboratory of Plant Development and Environmental Adaptation Biology Ministry of EducationSchool of Life SciencesShandong UniversityQingdao 266237China

The formation of lateral branches has an important and fundamental contribution to the remarkable developmental plasticity of plants,which allows plants to alter their architecture to adapt to the challenging environment *** Gibberellin(GA)phytohormones have been known to regulate the outgrowth of axillary meristems(AMs),but the specific molecular mechanisms remain *** we show that DELLA proteins regulate axillary bud formation by interacting and regulating the DNA-binding ability of SQUAMOSA-PROMOTER BINDING PROTEIN LIKE 9(SPL9),a micro RNA156-targeted squamosa promoter binding protein-like transcription ***9 participates in the initial regulation of axillary buds by repressing the expression of LATERAL SUPPRESSOR(LAS),a key regulator inthe initiation of AMs,and LAS contributes to the specific expression pattern of the GA deactivation enzyme GA2ox4,which is specifically expressed in the axils of leaves to form a low-GA cell niche in this anatomical ***,increasing GA levels in leaf axils by ectopically expressing the GA-biosynthesis enzyme GA20ox2 significantly impaired axillary meristem *** study demonstrates that DELLA-SPL9-LAS-GA2ox4 defines a core feedback regulatory module that spatially pattern GA content in the leaf axil and precisely control the axillary bud formation in different spatial and temporal.

关键词： SPL9 impaired spatially

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Brassinosteroids regulate outer ovule integument growth in part via the control of INNER NO OUTER by BRASSINOZOLE‐RESISTANT family transcription factors

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Journal of Integrative Plant Biology 2020年第8期62卷 1093-1111页

作者： Dandan Jia Lian-Ge Chen Guimin Yin Xiaorui Yang Zhihua Gao Yi Guo Yu Sun Wenqiang Tang Ministry of Education Key Laboratory of Molecular and Cellular Biology Hebei Collaboration Innovation Center for Cell SignalingHebei KeyLaboratory of Molecular and Cellular BiologyCollege of Life SciencesHebei Normal UniversityShijiazhuang 050024China College of Bioscience&Bioengineering Hebei University of Science and TechnologyShijiazhuang 050018China

Brassinosteroids(BRs)play important roles in regulating plant reproductive *** signaling or BR biosynthesis null mutants do not produce seeds under natural conditions,but the molecular mechanism underlying this infertility is poorly *** this study,we report that outer integument growth and embryo sac development were impaired in the ovules of the Arabidopsis thaliana BR receptor null mutant *** expression and RNA-seq analyses showed that the expression of INNER NO OUTER(INO),an essential regulator of outer integument growth,was significantly reduced in the bri1-116 *** INO expression due to overexpression or increased transcriptional activity of BRASSINAZOLE-RESISTANT 1(BZR1)in the mutant alleviated the outer integument growth defect in bri1-116 ovules,suggesting that BRs regulate outer integument growth partially via BZR1-mediated transcriptional regulation of ***,INO expression in bzr-h,a null mutant for all BZR1 family genes,was barely detectable;and the outer integument of bzr-h ovules had much more severe growth defects than those of the bri1-116 ***,our findings establish a new role for BRs in regulating ovule development and suggest that BZR1 family transcription factors might regulate outer integument growth through both BRI1-dependent and BRI1-independent pathways.

关键词： impaired outer steroids

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Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration

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Signal Transduction and Targeted Therapy 2021年第2期6卷 436-446页

作者： Rui Gong Zuke Jiang Naufal Zagidullin Tianyi Liu Benzhi Cai Department of Pharmacy at the Second Afliated Hospital and Department of Pharmacology(The Key Laboratory of Cardiovascular ResearchMinistry ol Education)at College of PharmacyHarbin Medical University150086 HarbinChina Department of Internal Diseases Bashkir State Medical UniversityUfa 450008Russia College of Pharmacy University of CincinnatiCincinnatiOHUSA

With the high morbidity and mortality rates,cardiovascular diseases have become one of the most concerning diseases *** heart of adult mammals can hardly regenerate naturally after injury because adult cardiomyocytes have already exited the cell cycle,which subseqently triggers cardiac remodeling and heart *** a series of pharmacological treatments and surgical methods have been utilized to improve heart functions,they cannot replenish the massive loss of beating cardiomyocytes after ***,we summarize the latest research progress in cardiac regeneration and heart repair through altering cardiomyocyte fate plasticity,which is emerging as an effective strategy to compensate for the loss of functional cardiomyocytes and improve the impaired heart ***,residual cardiomyocytes in damaged hearts re-enter the cell cycle to acquire the proliferative capacity by the modifications of cell cycle-related genes or regulation of growth-related ***,non-cardiomyocytes such as cardiac fbroblasts,were shown to be reprogrammed into cardiomyocytes and thus favor the repair of damaged ***,pluripotent stem cells have been shown to transform into cardiomyocytes to promote heart healing after myocardial infarction(MI).Furthermore,in vitro and in vivo studies demonstrated that environmental oxygen,energy metabolism,extracellular factors,nerves,non-coding RNAs,*** the key regulatory functions in cardiac *** fndings provide the theoretical basis of targeting cellular fate plasticity to induce cardiomyocyte proliferation or formation,and also provide the clues for stimulating heart repair after injury.

关键词： cardiac metabolism impaired

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CD 147 receptor is essential for TFF3-mediated signaling regulating colorectal cancer progression

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Signal Transduction and Targeted Therapy 2021年第8期6卷 2521-2535页

作者： Hong-Yong Cui Shi-Jie Wang Fei Song Xu Cheng Gang Nan Yu Zhao Mei-Rui Qian Xi Chen Jia-Yue Li Fen-Ling Liu Yu-Meng Zhu Ruo-Fei Tian Bin Wang Bin Wu Yang Zhang Xiu-Xuan Sun Ting Guo Xiang-Min Yang Hai Zhang Ling Li Jing Xu Hui-Jie Bian Jian-Li Jiang Zhi-Nan Chen National Translational Science Center for Molecular Medicine and Department of Cell Biology Fourth Military Medical UniversityXi'anChina Department of Urology Shenzhen Institute of Translational MedicineThe First Affiliated Hospital of Shenzhen UniversityShenzhen Second People's HospitalShenzhenChina Medical Research Institute School of MedicineWuhan UniversityWuhanChina College of Chemistry and Materials Science Northwest UniversityXi'anChina National Facility for Protein Science Shanghai Zhangjiang LabShanghai Advanced Research InstituteChinese Academy of SciencesShanghaiChina Medical Research Center Southern University of Science and Technology HospitalShenzhenChina

Major gaps in understanding the molecular mechanisms of colorectal cancer(CRC)progression and intestinal mucosal repair have hampered therapeutic development for gastrointestinal *** factor 3(TFF3)has been reported to be involved in CRC progression and intestinal mucosal repair;however,how TFF3 drives tumors to become more aggressive or metastatic and how TFF3 promotes intestinal mucosal repair are still poorly ***,we found that the upregulated TFF3 in CRC predicted a worse overall survival ***3 deficiency impaired mucosal restitution and ***147,a membrane protein,was identified as a binding partner for *** binding to CD147,TFF3 enhanced CD147-CD44s interaction,resulting in signal transducer and activator of transcription 3(STAT3)activation and prostaglandin G/H synthase 2(PTGS2)expression,which were indispensable for TFF3-induced migration,proliferation,and ***2-derived PGE2 bound to prostaglandin E2 receptor EP4 subtype(PTGER4)and contributed to TFF3-stimulated CRC *** NMR studies of the TFF3-CD147 interaction revealed the key residues critical for TFF3 binding and the induction of PTGS2 *** ability of TFF3 to enhance mucosal restitution was weakened by a PTGS2 *** of TFF3-CD147 signaling using competitive inhibitory antibodies or a PTGS2 inhibitor reduced CRC lung metastasis in *** findings bring strong evidence that CD147 is a novel receptor for TFF3 and PTGS2 signaling is critical for TFF3-induced mucosal restitution and CRC progression,which widens and deepens the understanding of the molecular function of trefoil factors.

关键词： TFF3 colorectal impaired

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Hypoxia-induced GBE1 expression promotes tumor progression through metabolic reprogramming in lung adenocarcinoma

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1807-1821页

作者： Lifeng Li Li Yang Zhirui Fan Wenhua Xue Zhibo Shen Yongliang Yuan Xiangdong Sun Dan Wang Jingyao Lian Liping Wang Jie Zhao Yi Zhang Biotherapy Center The First Affiliated Hospital of Zhengzhou University450052 ZhengzhouHenanChina Cancer Center The First Affiliated Hospital of Zhengzhou University450052 ZhengzhouHenanChina Internet Medical and System Applications of National Engineering Laboratory ZhengzhouChina Integrated Traditional and Western Medicine The First Affiliated Hospital of Zhengzhou University450052 ZhengzhouHenanChina Department of Pharmacy The First Affiliated Hospital of Zhengzhou University450052 ZhengzhouHenanChina Marshall B.J.Medical Research Centre Zhengzhou University450052 ZhengzhouHenanChina

Hypoxia mediates a metabolic switch from oxidative phosphorylation to glycolysis and increases glycogen *** previously found that glycogen branching enzyme(GBE1)is downstream of the hypoxia-inducible factor-1(HIF1)signaling pathway in lung adenocarcinoma(LUAD)cells;however,the molecular mechanism underlying HIF1 regulation of GBE1 expression remains ***,the effect of GBE1 on tumor progression via changes in metabolic signaling under hypoxia in vitro and in vivo was evaluated,and GBE1-related genes from human specimens and data sets were *** induced GBE1 upregulation in LUAD ***1-knockdown A549 cells showed impaired cell proliferation,clone formation,cell migration and invasion,angiogenesis,tumor growth,and ***1 mediated the metabolic reprogramming of LUAD *** expression of gluconeogenesis pathway molecules,especially fructose-1,6-bisphosphatase(FBP1),was markedly higher in shGBE1 A549 cells than it was in the control ***1 inhibited the tumor progression of ***1-mediated FBP1 suppression via promoter methylation enhanced HIF1αlevels through NF-κB ***1 may be a negative prognostic biomarker for LUAD ***,hypoxia-induced HIF1αmediated GBE1 upregulation,suppressing FBP1 expression by promoter methylation via NF-κB signaling in LUAD ***1 blockade upregulated HIF1α,triggered the switch to anaerobic glycolysis,and enhanced glucose ***,targeting HIF1α/GBE1/NF-κB/FBP1 signaling may be a potential therapeutic strategy for LUAD.

关键词： GBE adenocarcinoma impaired

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The Use of High-Throughput Phenotyping for Assessment of Heat Stress-Induced Changes in Arabidopsis

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Plant Phenomics 2020年第1期2卷 196-209页

作者： Ge Gao Mark A.Tester Magdalena M.Julkowska Division of Biological and Environmental Sciences and Engineering(BESE) King Abdullah University of Science and Technology(KAUST)Thuwal 23955-6900Saudi Arabia

The worldwide rise in heatwave frequency poses a threat to plant survival and *** the new marker phenotypes that show reproducible response to heat stress and contribute to heat stress tolerance is becoming a *** this study,we describe a protocol focusing on the daily changes in plant morphology and photosynthetic performance after exposure to heat stress using an automated noninvasive phenotyping *** stress exposure resulted in an acute reduction of the quantum yield of photosystem II and increased leaf *** longer term,the exposure to heat also affected plant growth and *** tracking the recovery period of the WT and mutants impaired in thermotolerance(hsp101),we observed that the difference in maximum quantum yield,quenching,rosette size,and *** examining the correlation across the traits throughout time,we observed that early changes in photochemical quenching corresponded with the rosette size at later stages,which suggests the contribution of quenching to overall heat *** also determined that 6 h of heat stress provides the most informative insight in plant’s responses to heat,as it shows a clear separation between treated and nontreated plants as well as the WT and *** work streamlines future discoveries by providing an experimental protocol,data analysis pipeline,and new phenotypes that could be used as targets in thermotolerance screenings.

关键词： quenching impaired separation

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