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TMEM63B regulates postnatal development of cochlear sensory epithelia via thyroid hormone signaling

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Journal of Genetics and Genomics 2024年第6期51卷 673-676页

作者： Chang Ye Tian-Zi Zhang Yan-Yu Zang Yun Stone Shi Guoqiang Wan state key laboratory of pharmaceutical biotechnology and moe key laboratory of model Animal for disease study Model Animal Research CenterMedical SchoolNanjing UniversityNanjingJiangsu 210032China Guangdong Institute of Intelligence Science and Technology ZhuhaiGuangdong 519031China

Sound transmission occurs in the cochlea,a complex and ingenious subdivision in the inner *** structure of the cochlea develops structurally and functionally by the time before two postnatal weeks(the time of hearing onset)in mice(Geal-Dor et al.,1993).Greater epithelial ridge(GER,also known as Kolliker's organ)is a transient cochlear structure containing a group of columnar epithelial supporting cells surrounding the inner hair cells(IHCs).

关键词： cochlear al. supporting

TBC1D1 is an energy-responsive polarization regulator of macrophages via governing ROS production in obesity

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Science China Life Sciences 2024年第9期67卷 1899-1914页

作者： Qi Wang Ping Rong Wen Zhang Xinyu Yang Liang Chen Ye Cao Minjun Liu Weikuan Feng Qian Ouyang Qiaoli Chen Hailong Li Hui Liang Fanguo Meng Hong-Yu Wang Shuai Chen state key laboratory of pharmaceutical biotechnology Department of Cardiology Nanjing Drum Tower Hospital The Affiliated Hospital of Nanjing University Medical School Model Animal Research CenterSchool of Medicine Nanjing University moe key laboratory of model Animal for disease study Department of Endocrinology Nanjing Drum Tower Hospital The Affiliated Hospital of Nanjing University Medical School Model Animal Research Center School of Medicine Nanjing University College of Life Science Anhui Medical University Redox Medical Center for Public Health Medical College of Soochow University Department of General Surgery First Affiliated Hospital Nanjing Medical University

Energy status is linked to the production of reactive oxygen species（ROS） in macrophages, which is elevated in obesity. However, it is unclear how ROS production is upregulated in macrophages in response to energy overload for mediating the development of obesity. Here,we show that the Rab-GTPase activating protein（Rab GAP） TBC1D1, a substrate of the energy sensor AMP-activated protein kinase（AMPK）,is a critical regulator of macrophage ROS production and consequent adipose inflammation for obesity development. TBC1D1 deletion decreases, whereas an energy overload-mimetic non-phosphorylatable TBC1D1S231AAmutation increases, ROS production and M1-like polarization in macrophages. Mechanistically, TBC1D1 and its downstream target Rab8a form an energy-responsive complex with NOX2 for ROS generation. Transplantation of TBC1D1S231Abone marrow aggravates diet-induced obesity whereas treatment with an ultra-stable Tt SOD for removal of ROS selectively in macrophages alleviates both TBC1D1S231Amutation-and diet-induced obesity. Our findings therefore have implications for drug discovery to combat obesity.

关键词： TBC1D1 AMPK Rab8a NOX2 ROS inflammation macrophage obesity

LonP1 Links Mitochondria–ER Interaction to Regulate Heart Function

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Research 2024年第1期2023卷 595-609页

作者： Yujie Li Dawei Huang Lianqun Jia Fugen Shangguan Shiwei Gong Linhua Lan Zhiyin Song Juan Xu Chaojun Yan Tongke Chen Yin Tan Yongzhang Liu Xingxu Huang Carolyn K.Suzuki Zhongzhou Yang Guanlin Yang Bin Lu The Affiliated Nanhua Hospital and School of Basic Medical Sciences Hengyang Medical SchoolUniversity of South ChinaHengyangHunan 421001China School of laboratory Medicine and Life Sciences Wenzhou Medical UniversityWenzhouZhejiang 325035China National Health Commission key laboratory of Birth Defect Research and Prevention Hunan Provincial Maternal and Child Health Care HospitalChangshaHunan 410008China key laboratory of Ministry of Education for TCM Viscera-state Theory and Applications Ministry of Education of ChinaLiaoning University of Traditional Chinese MedicineShenyangLiaoning 110847China key laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic diseases of Zhejiang Province The First Affiliated Hospital of Wenzhou Medical UniversityWenzhouZhejiangChina Hubei key laboratory of Cell Homeostasis College of Life SciencesWuhan UniversityWuhanHubei 430072China Nanjing Maternity and Child Health Care Hospital Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical UniversityNanjing 210004China Animal Center Wenzhou Medical UniversityWenzhouZhejiang 325035China Department of Cardiology The First Affiliated Hospital of University of South ChinaHengyangHunanChina School of Life Science and Technology Shanghai Tech UniversityShanghai 201210China Department of Microbiology Biochemistry and Molecular GeneticsNew Jersey Medical School-RutgersThe State University of New JerseyNewarkNJUSA state key laboratory of pharmaceutical biotechnology Department of CardiologyNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical School and MOE Key Laboratory of Model Animal for Disease StudyModel Animal Research CenterNanjing UniversityNanjing 210061China

Interorganelle contacts and communications are increasingly recognized to play a vital role in cellular function and *** particular,the mitochondria–endoplasmic reticulum(ER)membrane contact site(MAM)is known to regulate ion and lipid transfer,as well as signaling and organelle ***,the regulatory mechanisms of MAM formation and their function are still ***,we identify mitochondrial Lon protease(LonP1),a highly conserved mitochondrial matrix protease,as a new MAM tethering *** removal of LonP1 substantially reduces MAM formation and causes mitochondrial ***,deletion of LonP1 in the cardiomyocytes of mouse heart impairs MAM integrity and mitochondrial fusion and activates the unfolded protein response within the ER(UPR^(ER)).Consequently,cardiac-specific LonP1 deficiency causes aberrant metabolic reprogramming and pathological heart *** findings demonstrate that LonP1 is a novel MAM-localized protein orchestrating MAM integrity,mitochondrial dynamics,and UPR^(ER),offering exciting new insights into the potential therapeutic strategy for heart failure.

关键词： offering programming insight

E3 ligase Herc4 regulates Hedgehog signalling through promoting Smoothened degradation

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Journal of Molecular Cell Biology 2019年第9期11卷 791-803页

作者： Weirong jiang Xia Yao Zhaoliang Shan Wenting Li Yuxue Gao Qing Zhang state key laboratory of pharmaceutical biotechnology and moe key laboratory of model animals for disease study Model Animal Research Center of Nanjing UniversityNanjing 210061China

Hedgehog(Hh)signalling plays conserved roles in controlling embryonic development;its dysregulation causes many diseases including *** G protein-coupled receptor Smoothened(Smo)is the key signal transducer of the Hh pathway,whose posttranslational regulation has been shown to be critical for its accumulation and *** has been reported an essential posttranslational regulation of ***,we identify a novel E3 ligase of Smo,Herc4,which binds to Smo,and regulates Hh signalling by controlling Smo ubiquitination and ***,our data suggest that Herc4-mediated Smo degradation is regulated by Hh in PKA-primed phosphorylation-dependent and independent manners.

关键词： Hedgehog Smoothened Herc4 ubiquitination

Comments on ‘FNIP1 regulates adipocyte browning and systemic glucose homeostasis in mice by shaping intracellular calcium dynamics'

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Journal of Molecular Cell Biology 2022年第5期14卷 60-62页

作者： Yujing Yin Dengqiu Xu Yan Mao Zhenji Gan state key laboratory of pharmaceutical biotechnology and moe key laboratory of model Animal for disease study Division of Spine SurgeryDepartment of Orthopedic SurgeryNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolJiangsu Key Laboratory of Molecular MedicineChemistry and Biomedicine Innovation Center(ChemBIC)Model Animal Research CenterNanjing University Medical SchoolNanjing UniversityNanjing 210061China

Owing to its remarkable benefits on metabolic health and its demonstrated presence in adult humans,beige or‘brite'adipocytes holdgreatpromiseto combat obesity and metabolic *** of the mechanisms involved inadipocyte... 详细信息

关键词： adipocyte homeostasis obesity

Deficiency of Autophagy-Related Gene 5 in Keratinocytes Leads to Aggravation of Epidermal Damage in 2,4-Dinitrochlorobenzene-Induced Allergic Contact Dermatitis

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International Journal of Dermatology and Venereology 2023年第4期6卷 214-223页

作者： Yi-Qun Zhang Ta Xiao Chang-Jun Song Yang-Ying Ke Xiang Gao Min Li Heng Gu Xu Chen Jiangsu key laboratory of Molecular Biology for Skin diseases and STIs Hospital for Skin Diseases(Institute of Dermatology)Chinese Academy of Medical Sciences&Peking Union Medical CollegeNanjingJiangsu 210042China state key laboratory of pharmaceutical biotechnology MOE Key Laboratory of Model Animals for Disease StudyJiangsu Key Laboratory of Molecular MedicineModel Animal Research CenterNational Resource Center for Mutant Mice of ChinaSchool of MedicineNanjing UniversityNanjingJiangsu 210061China School of Public Health Nanjing Medical UniversityNanjingJiangsu 211166China key laboratory of Basic and Translational Research on Immune-Mediated Skin diseases Chinese Academy of Medical SciencesNanjingJiangsu 210042China.

Objective:The interrelationship between apoptosis and autophagy plays an important role in many pathophysiological processes,however,whether their interplay is involved in allergic contact dermatitis(ACD)has not yet been ***,we conducted this study to determine whether keratinocyte-specific autophagy-related gene 5(ATG5)deficiency can regulate apoptosis to inhibit skin damage in mice with 2,4-dinitrochlorobenzene(DNCB)-induced ***:This study involved keratinocyte-specificAtg5 conditional knockout(cKO)mice(Krt14cre/+-Atg5flox/flox)and control mice(Krt14+/+-Atg5flox/flox).We painted DNCB on the right ear of each mouse to induce *** scoring and measurements of ear weight and thickness were performed to evaluate inflammation *** immunohistochemical assay was performed to analyze immune cell *** study and TUNEL staining were performed to compare the differences in skin lesions betweenAtg5 cKO mice and control *** and western blotting were used to examine the levels of ATG5 and apoptosis-related *** results were statistically analyzed byt ***:After DNCB stimulation of mice ears,we observed a more severe phenotype inAtg5 cKO mice than in control mice(dermatitis score:7.500±2.588vs.3.250±0.822,P=0.003).Further analysis of ATG5 protein confirmed keratinocyte-specific ablation ofAtg5 in cKO mice and showed that DNCB did not influence ATG5 *** assay revealed that the infiltrated immune cells were not involved in aggravation of the phenotype of DNCB-stimulatedAtg5 cKO ***,the histological study(P=0.024),TUNEL staining(P=0.024),immunofluorescence(P=0.036),and western blotting showed that the increase in keratinocyte death,especially apoptosis,contributed to aggravation of the phenotype of DNCB-stimulatedAtg5 cKO ***:Deficiency ofAtg5 in keratinocytes increases apoptosis,aggravating skin damage in DNCB-induced ACD *** has no relation

关键词： allergic contact dermatitis autophagy-related gene 5 apoptosis autophagy

SERCA regulates collective cell migration by maintaining cytoplasmic Ca2+ homeostasis

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Journal of Genetics and Genomics 2019年第9期46卷 451-454页

作者： Xuan Guo Jun Luo Heng Wang Jiong Chen state key laboratory of pharmaceutical biotechnology and moe key laboratory of model animals for disease study Model Animal Research CenterNanjing UniversityNanjing210061China College of Life Science Shangrao Normal UniversityShangrao334001China

Characterized by multicellular migratory behavior and cooperative ability,collective cell migration plays critical roles in developmental,physiological and pathological processes,such as organogenesis,wound healing and tumor metastasis (Friedl and Gilmour,2009).Molecular features of collective cell migration including collective polarization,coordinated cytoskeletal activity,and guidance signaling have been recently investigated in a variety of in vivo and in vitro model systems (Scarpa and Mayor,2016),but many other aspects of regulatory mechanisms remain unexplored.

关键词： homeostasis healing collective

Impaired SERCA2a phosphorylation causes diabetic cardiomyopathy through impinging on cardiac contractility and precursor protein processing

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Life Metabolism 2022年第1期1卷 54-66页

作者： Chao Quan Sangsang Zhu Ruizhen Wang Jiamou Chen Qiaoli Chen Min Li Shu Su Qian Du Minjun Liu Hong-Yu Wang Shuai Chen moe key laboratory of model Animal for disease study Department of CardiologyNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolModel Animal Research CenterSchool of MedicineNanjing UniversityNanjingJiangsu 210061China state key laboratory of pharmaceutical biotechnology Department of EndocrinologyNanjing Drum Tower HospitalModel Animal Research CenterSchool of MedicineNanjing UniversityNanjingJiangsu 210061China Jiangsu key laboratory of Molecular Medicine Model Animal Research CenterSchool of MedicineNanjing UniversityNanjing 210061China

Diabetic cardiomyopathy(DCM)is currently a progressive and nonstoppable complication in type 2 diabetic *** insults and insulin resistance are involved in its pathogenesis;however,the underlying mechanisms are still not clearly *** we show that calcium dysregulation can be both a cause and a consequence of cardiac insulin resistance that leads to DCM.A western diet induces the development of DCM through at least three phases in mice,among which an early phase depends on impaired Thr^(484)-phosphorylation of sarcoplasmic/endoplasmic reticulum calcium ATPase 2a(SERCA2a)elicited by insulin *** of SERCA2a-Thr^(484) to a nonphosphorylatable alanine delays calcium re-uptake into the sarcoplasmic reticulum in the cardiomyocytes and decreases cardiac function at the ***,this mutation blunts the early phase of DCM,but has no effect on disease progression in the following ***,impairment of sarcoplasmic reticulum calcium re-uptake caused by the SERCA2a-Thr^(484) mutation inhibited processing of insulin receptor precursor through FURIN convertase,resulting in cardiac insulin ***,these data reveal a bidirectional relationship between insulin resistance and impairment of calcium homeostasis,which may underlie the early pathogenesis of *** findings have therapeutic implications for early intervention of DCM.

关键词： SERCA SPEG phosphorylation calcium insulin diabetic cardiomyopathy

Master microRNA-222 regulates cardiac microRNA maturation and triggers Tetralogy of Fallot

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Signal Transduction and Targeted Therapy 2022年第6期7卷 1895-1898页

作者： Chao Li Hongdou Li Xiaoying Yao Dong Liu Yongming Wang Xinyi Huang Zhongzhou Yang Wufan Tao Jian-Yuan Zhao Hongyan Wang Obstetrics and Gynecology Hospital NHC Key Laboratory of Reproduction RegulationShanghai Institute of Planned Parenthood ResearchState Key Laboratory of Genetic EngineeringSchool of Life Sciencesand Children’s HospitalFudan University200438 ShanghaiChina Shanghai key laboratory of Metabolic Remodeling and Health Institute of Metabolism and Integrative BiologyInstitute of Reproduction and DevelopmentFudan University200438 ShanghaiChina School of Life Science Key Laboratory of Neuroregeneration of Jiangsu and Ministry of EducationCo-innovation Center of NeuroregenerationNantong University226019 NantongChina state key laboratory of pharmaceutical biotechnology and moe key laboratory of model Animal for disease study Nanjing University Medical School211166 NanjingChina Institute of Developmental Biology&Molecular Medicine Fudan University200438 ShanghaiChina

Dear Editor,Tetralogy of Fallot(TOF)is the most common complex congenital heart *** gene mutations and copy number variants,altered protein function induced by posttranscriptional or translational regulation also contributes to the onset of TOF.1 MiRNAs are short noncoding RNAs that bind to the 3’-UTR of target mRNAs to repress protein ***,the causal link between miRNAs and TOF and the underlying mechanism has not been established.

关键词： Fallot congenital cardiac