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Bone Research 2024年第1期12卷 122-136页

作者： Nan-Yu Zou Ran Liu Mei Huang Yu-Rui Jiao Jie Wei Yangzi Jiang Wen-Zhen He Min Huang Yi-Li Xu Ling Liu Yu-Chen Sun Mi Yang Qi Guo Yan Huang Tian Su Ye Xiao Wei-Shan Wang Chao Zeng Guang-Hua Lei Xiang-Hang Luo Chang-Jun Li Department of endocrinology Endocrinology Research CenterXiangya Hospital of Central South UniversityChangshaHunan 410008China Department of Orthopaedics Xiangya Hospital of Central South UniversityChangshaHunan 410008China Department of Epidemiology and Health Statistics Xiangya School of Public HealthCentral South UniversityChangshaChina Hunan key laboratory of Joint Degeneration and Injury ChangshaHunan 410008China key laboratory of Aging-related Bone and Joint Diseases Prevention and Treatment Ministry of EducationXiangya HospitalCentral South UniversityChangshaChina School of Biomedical Sciences Institute for Tissue Engineering and Regenerative MedicineFaculty of MedicineThe Chinese University of Hong KongHong Kong SARChina Department of Orthopaedics The First Affiliated Hospital of Shihezi UniversityShiheziXinjiangChina National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangshaHunan 410008China

Skeletal stem/progenitor cell(SSPC)senescence is a major cause of decreased bone regenerative potential with aging,but the causes of SSPC senescence remain unclear.In this study,we revealed that macrophages in calluses secrete prosenescent factors,including grancalcin(GCA),during aging,which triggers SSPC senescence and impairs fracture healing.Local injection of human rGCA in young mice induced SSPC senescence and delayed fracture repair.Genetic deletion of Gca in monocytes/macrophages was sufficient to rejuvenate fracture repair in aged mice and alleviate SSPC senescence.Mechanistically,GCA binds to the plexin-B2 receptor and activates Arg2-mediated mitochondrial dysfunction,resulting in cellular senescence.Depletion of Plxnb2 in SSPCs impaired fracture healing.Administration of GCA-neutralizing antibody enhanced fracture healing in aged mice.Thus,our study revealed that senescent macrophages within calluses secrete GCA to trigger SSPC secondary senescence,and GCA neutralization represents a promising therapy for nonunion or delayed union in elderly individuals.

关键词： healing union senescence

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A novel preimplantation genetic testing strategy for a subtelomeric genetic disorder:A case study

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Genes & Diseases 2024年第4期11卷 13-15页

作者： Songchang Chen Li Wanng Luting Chen Weihui Shi Junyu Zhang Yuting Hu Yinyu Wang Li Jin Jianzhong Sheng Feng Zhang Yanting Wu Hefeng Huang Chenming Xu Obstetrics and Gynecology Hospital Institute of Reproduction and DevelopmentFudan UniversityShanghai 200090China The International Peace Maternity and Child Health Hospital School of MedicineShanghai Jiao Tong UniversityShanghai 200030China Research Units of Embryo Original Diseases Chinese Academy of Medical SciencesShanghai 200030China key laboratory of Reproductive Genetics(Ministry of Education) Department of Reproductive EndocrinologyWomen's HospitalZhejiang University School of MedicineHangzhouZhejiang 310058China Shanghai key laboratory of Embryo Original Diseases Shanghai 200030China Shanghai First Maternity and Infant Hospital Tongji University School of MedicineShanghai 200030China

Preimplantation genetic testing(PGT)is a precise and effective technique for detecting inherited pathogenic mutations to prevent birth defects.However,there are few reports on PGT for pseudo-autosomal genetic diseases.

关键词： implantation testing precise

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Deleterious variants in RNF111 impair female fertility and induce premature ovarian insufficiency in humans and mice

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Science China(Life Sciences) 2024年第7期67卷 1325-1337页

作者： Chengcheng Song Yingying Qin Yan Li Bingyi Yang Ting Guo Wenqing Ma Dian Xu keyan Xu Fangfang Fu Li Jin Yanhua Wu Shuyan Tang Xiaojun Chen Feng Zhang Obstetrics and Gynecology Hospital State Key Laboratory of Genetic EngineeringInstitute of Medical Genetics and GenomicsFudan UniversityShanghai 200011China Human Phenome Institute Zhangjiang Fudan International Innovation CenterFudan UniversityShanghai 201203China Center for Reproductive Medicine Cheeloo College of MedicineShandong UniversityJinan 250021China State key laboratory of Reproductive Medicine and Offspring Health Key Laboratory of Reproductive Endocrinology of Ministry of EducationNational Research Center for Assisted Reproductive Technology and Reproductive GeneticsShandong Key Laboratory of Reproductive MedicineShandong Provincial Clinical Research Center for Reproductive HealthShandong UniversityJinan 250021China Department of Obstetrics and Gynecology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China National Demonstration Center for Experimental Biology Education School of Life SciencesFudan UniversityShanghai 200433China Department of Gynecology the Tenth People’s Hospital of Tongji UniversityShanghai 200072China Soong Ching Ling Institute of Maternity and Child Health International Peace Maternity and Child Health Hospital of China Welfare InstituteShanghai 200030China

Premature ovarian insufficiency(POI)is a heterogeneous female disorder characterized by the loss of ovarian function before the age of 40.It represents a significant detriment to female fertility.However,the known POI-causative genes currently account for only a fraction of cases.To elucidate the genetic factors underlying POI,we conducted whole-exome sequencing on a family with three fertile POI patients and identified a deleterious missense variant in RNF111.In a subsequent replication study involving 1,030 POI patients,this variant was not only confirmed but also accompanied by the discovery of three additional predicted deleterious RNF111 variants.These variants collectively account for eight cases,representing 0.78%of the study cohort.A further study involving 500 patients with diminished ovarian reserve also identified two additional RNF111 variants.Notably,RNF111 encodes an E3 ubiquitin ligase with a regulatory role in the TGF-β/BMP signaling pathway.Our analysis revealed that RNF111/RNF111 is predominantly expressed in the oocytes of mice,monkeys,and humans.To further investigate the functional implications of RNF111 variants,we generated two mouse models:one with a heterozygous missense mutation(Rnf111+/M)and another with a heterozygous null mutation(Rnf111^(+/-)).Both mouse models exhibited impaired female fertility,characterized by reduced litter sizes and small ovarian reserve.Additionally,RNA-seq and quantitative proteomics analysis unveiled that Rnf111 haploinsufficiency led to dysregulation in female gonad development and negative regulation of the BMP signaling pathway within mouse ovaries.In conclusion,our findings strongly suggest that monoallelic deleterious variants in RNF111 can impair female fertility and induce POI in both humans and mice.

关键词： POI RNF111 female fertility ovarian reserve

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Unveiling the role of hypoxia-inducible factor 2alpha in osteoporosis:Implications for bone health

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World Journal of Stem Cells 2024年第4期16卷 389-409页

作者： Ling-Ling Wang Zhan-Jin Lu Shun-Kui Luo Yun Li Zhe Yang Hong-Yun Lu Department of Gerontology The Fifth Affiliated Hospital of Sun Yat-sen UniversityZhuhai 519000Guangdong ProvinceChina Department of endocrinology and Metabolism The Fifth Affiliated Hospital of Sun Yat-sen UniversityZhuhai 519000Guangdong ProvinceChina Guangdong Provincial key laboratory of Biomedical Imaging The Fifth Affiliated Hospital of Sun Yat-sen UniversityZhuhai 519000Guangdong ProvinceChina Department of endocrinology and Metabolism Zhuhai People’s Hospital(Zhuhai Clinical Medical College of Jinan Universitythe First Hospital Affiliated with Medical College of Macao University of Science and Technology)Zhuhai 519000Guangdong ProvinceChina

BACKGROUND Osteoporosis(OP)has become a major public health problem worldwide.Most OP treatments are based on the inhibition of bone resorption,and it is necessary to identify additional treatments aimed at enhancing osteogenesis.In the bone marrow(BM)niche,bone mesenchymal stem cells(BMSCs)are exposed to a hypoxic environment.Recently,a few studies have demonstrated that hypoxiainducible factor 2alpha(HIF-2α)is involved in BMSC osteogenic differentiation,but the molecular mechanism involved has not been determined.AIM To investigate the effect of HIF-2αon the osteogenic and adipogenic differentiation of BMSCs and the hematopoietic function of hematopoietic stem cells(HSCs)in the BM niche on the progression of OP.METHODS Mice with BMSC-specific HIF-2αknockout(Prx1-Cre;Hif-2αfl/fl mice)were used for in vivo experiments.Bone quantification was performed on mice of two genotypes with three interventions:Bilateral ovariectomy,semilethal irradiation,and dexamethasone treatment.Moreover,the hematopoietic function of HSCs in the BM niche was compared between the two mouse genotypes.In vitro,the HIF-2αagonist roxadustat and the HIF-2αinhibitor PT2399 were used to investigate the function of HIF-2αin BMSC osteogenic and adipogenic differentiation.Finally,we investigated the effect of HIF-2αon BMSCs via treatment with the mechanistic target of rapamycin(mTOR)agonist MHY1485 and the mTOR inhibitor rapamycin.RESULTS The quantitative index determined by microcomputed tomography indicated that the femoral bone density of Prx1-Cre;Hif-2αfl/fl mice was lower than that of Hif-2αfl/fl mice under the three intervention conditions.In vitro,Hif-2αfl/fl mouse BMSCs were cultured and treated with the HIF-2αagonist roxadustat,and after 7 d of BMSC adipogenic differentiation,the oil red O staining intensity and mRNA expression levels of adipogenesis-related genes in BMSCs treated with roxadustat were decreased;in addition,after 14 d of osteogenic differentiation,BMSCs treated with roxadustat exhibited increased expression of osteogenesis

关键词： Hypoxia-inducible factor-2α Bone marrow niche Bone mesenchymal stem cells Osteoporosis Osteogenic/adipogenic differentiation Mechanistic target of rapamycin signaling pathway

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Cronkhite-Canada syndrome with esophagus involvement and sixyear follow-up:A case report

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World Journal of Gastroenterology 2024年第8期30卷 984-990页

作者： Yu-Chen Tang Department of endocrinology The First Affiliated Hospital of Ningbo UniversityNingbo 315000Zhejiang ProvinceChina

BACKGROUND Cronkhite-Canada syndrome(CCS)is a rare,noninherited disease characterized by gastrointestinal polyposis with diarrhea and ectodermal abnormalities.CCS polyps are distributed through the whole digestive tract,and they are common in the stomach and colon but very uncommon in the esophagus.CASE SUMMARY Here,we present a case of a 63-year-old man with skin hyperpigmentation accompanied by diarrhea,alopecia,and loss of his fingernails.laboratory data indicated anemia,hypoalbuminemia,hypocalcemia,hypokalemia,and positive fecal occult blood.Endoscopy showed numerous polyps scattered throughout the digestive tract,including the esophagus.He was treated with nutritional support and glucocorticoids with remission of his symptoms.CONCLUSION Comprehensive treatment led by hormonal therapy can result in partial or full remission of clinical symptoms.Treatment should be individualized for each patient according to their therapy response.Surveillance endoscopy is necessary for assessing mucosal disease activity and detecting malignant transformation.

关键词： Cronkhite-Canada syndrome Gastrointestinal polyposis Hormonal therapy Prognosis Case report

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Role of deubiquitinase JOSD2 in the pathogenesis of esophageal squamous cell carcinoma

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World Journal of Gastroenterology 2024年第6期30卷 565-578页

作者： Wen-Peng Wang Dan Shi Duo Yun Jun Hu Jie-Fu Wang Jia Liu Yan-Peng Yang Ming-Rui Li Jun-FengWang Da-Lu Kong Department of Colorectal Oncology Tianjin Medical University Cancer Institute and HospitalNational Clinical Research Center for CancerTianjin’s Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjin 300060China Department of Gastrointestinal Surgery Tianjin Nan Kai HospitalTianjin Medical UniversityTianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM RepairInstitute of Integrative Medicine for Acute Abdominal DiseasesTianjin 300100China Department of Oncology The First Hospital of HohhotHohhot 010000Inner Mongolia Autonomous RegionChina Department of endocrinology Dazhou Central HospitalDazhou 635000Sichuan ProvinceChina

BACKGROUND Esophageal squamous cell carcinoma(ESCC)is a deadly malignancy with limited treatment options.Deubiquitinases(DUBs)have been confirmed to play a crucial role in the development of malignant tumors.JOSD2 is a DUB involved in con-trolling protein deubiquitination and influencing critical cellular processes in cancer.AIM To investigate the impact of JOSD2 on the progression of ESCC.METHODS Bioinformatic analyses were employed to explore the expression,prognosis,and enriched pathways associated with JOSD2 in ESCC.Lentiviral transduction was utilized to manipulate JOSD2 expression in ESCC cell lines(KYSE30 and RESULTS )Preliminary research indicated that JOSD2 was highly expressed in ESCC tissues,which was associated with poor prognosis.Further analysis demonstrated that JOSD2 was upregulated in ESCC cell lines compared to normal esophageal cells.JOSD2 knockdown inhibited ESCC cell activity,including proliferation and colony-forming ability.Moreover,JOSD2 knockdown decreased the drug resistance and migration of ESCC cells,while JOSD2 overexpression enhanced these phenotypes.In vivo xenograft assays further confirmed that JOSD2 promoted tumor proliferation and drug resistance in ESCC.Mechanistically,JOSD2 appears to activate the MAPK/ERK and PI3K/AKT signaling pathways.Mass spectrometry was used to identify crucial substrate proteins that interact with JOSD2,which identified the four primary proteins that bind to JOSD2,namely USP47,IGKV2D-29,HSP90AB1,and PRMT5.CONCLUSION JOSD2 plays a crucial role in enhancing the proliferation,migration,and drug resistance of ESCC,suggesting that JOSD2 is a potential therapeutic target in ESCC.

关键词： Esophageal squamous cell carcinoma JOSD2 Ubiquitination Biomarker Targeted therapy Drug resistance

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Unraveling the complexity of polycystic ovary syndrome with animal models

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Journal of Genetics and Genomics 2024年第2期51卷 144-158页

作者： Huanju Liu Mixue Tu Zhiyong Yin Dan Zhang Jun Ma Feng He Center for Genetic Medicine The Fourth Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang 310058China key laboratory of Women's Reproductive Health of Zhejiang Province and Department of Reproductive endocrinology Women's HospitalZhejiang University School of MedicineHangzhouZhejiang 310006China Zhejiang Provincial Clinical Research Center for Child Health Women's HospitalZhejiang University School of MedicineHangzhouZhejiang 310006China Clinical Research Center on Birth Defect Prevention and Intervention of Zhejiang Province HangzhouZhejiang 310006China Institute of Genetics Zhejiang University International School of MedicineHangzhouZhejiang 310058China Zhejiang Provincial key laboratory of Genetic and Developmental Disorder HangzhouZhejiang 310058China

Polycystic ovary syndrome (PCOS) is a highly familial and heritable endocrine disorder. Over half of the daughters born to women with PCOS may eventually develop their own PCOS-related symptoms. Progress in the treatment of PCOS is currently hindered by the complexity of its clinical manifestations and incomplete knowledge of its etiopathogenesis. Various animal models, including experimentally induced, naturally occurring, and spontaneously arising ones, have been established to emulate a wide range of phenotypical and pathological traits of human PCOS. These studies have led to a paradigm shift in understanding the genetic, developmental, and evolutionary origins of this disorder. Furthermore, emerging evidence suggests that animal models are useful in evaluating state-of-the-art drugs and treatments for PCOS. This review aims to provide a comprehensive summary of recent studies of PCOS in animal models, highlighting the power of these disease models in understanding the biology of PCOS and aiding high-throughput approaches.

关键词： Polycystic ovary syndrome Animal model Genetc manipulation Developmnental progtanning Drug screening

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Type 2 diabetes in children and adolescents:Exploring the disease heterogeneity and research gaps to optimum management

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World Journal of Clinical Pediatrics 2024年第2期13卷 80-99页

作者： Subhodip Pramanik Sunetra Mondal Rajan Palui Sayantan Ray Department of endocrinology Neotia Getwel Multi-specialty hospitalSiliguri 734010West BengalIndia Department of endocrinology NRS Medical College and HospitalKolkata 700014West BengalIndia Department of endocrinology All India Institute of Medical SciencesBhubaneswarBhubaneswar 751019OdishaIndia

Over the past 20 years,the incidence and prevalence of type 2 diabetes mellitus(T2DM)in children and adolescents have increased,particularly in racial and ethnic minorities.Despite the rise in T2DM in children and adolescents,the pathophysiology and progression of disease in this population are not clearly understood.Youth-onset T2DM has a more adverse clinical course than is seen in those who develop T2DM in adulthood or those with T1DM.Furthermore,the available therapeutic options are more limited for children and adolescents with T2DM compared to adult patients,mostly due to the challenges of implementing clinical trials.A better understanding of the mechanisms underlying the development and aggressive disease phenotype of T2DM in youth is important to finding effective prevention and management strategies.This review highlights the key evidence about T2DM in children and adolescents and its current burden and challenges both in clinical care and research activities.

关键词： Type 2 diabetes mellitus Children and adolescents Pathophysiology Heterogeneity Complications Treatment options Barriers

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Glucagon-like peptide 1 receptor activation:anti-inflammatory effects in the brain

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Neural Regeneration Research 2024年第8期19卷 1671-1677页

作者： Yolanda Diz-Chaves Zainab Maastor Carlos Spuch José Antonio Lamas Lucas C.González-Matías Federico Mallo Biomedical Research Centre(CINBIO) Laboratory of EndocrinologyUniversity of VigoGalicia Sur Health Research InstituteVigoSpain Translational Neuroscience Research Group Galicia Sur Health Research InstituteCIBERSAMHospitalÁlvaro CunqueiroSala InvestigaciónEstrada Clara CampoamorVigoSpain Biomedical Research Centre(CINBIO) Laboratory of NeuroscienceUniversity of VigoGalicia Sur Health Research InstituteVigoSpain

The glucagon-like peptide 1 is a pleiotropic hormone that has potent insulinotropic effects and is key in treating metabolic diseases such as diabetes and obesity.Glucagon-like peptide 1 exerts its effects by activating a membrane receptor identified in many tissues,including diffe rent brain regions.Glucagon-like peptide 1 activates several signaling pathways related to neuroprotection,like the support of cell growth/survival,enhancement promotion of synapse formation,autophagy,and inhibition of the secretion of proinflammatory cytokines,microglial activation,and apoptosis during neural morphogenesis.The glial cells,including astrocytes and microglia,maintain metabolic homeostasis and defe nse against pathogens in the central nervous system.After brain insult,microglia are the first cells to respond,followed by reactive astrocytosis.These activated cells produce proinflammato ry mediators like cytokines or chemokines to react to the insult.Furthermore,under these circumstances,mic roglia can become chro nically inflammatory by losing their homeostatic molecular signature and,consequently,their functions during many diseases.Several processes promote the development of neurological disorders and influence their pathological evolution:like the formation of protein aggregates,the accumulation of abnormally modified cellular constituents,the formation and release by injured neurons or synapses of molecules that can dampen neural function,and,of critical impo rtance,the dysregulation of inflammato ry control mechanisms.The glucagonlike peptide 1 receptor agonist emerges as a critical tool in treating brain-related inflammatory pathologies,restoring brain cell homeostasis under inflammatory conditions,modulating mic roglia activity,and decreasing the inflammato ry response.This review summarizes recent advances linked to the anti-inflammato ry prope rties of glucagon-like peptide 1 receptor activation in the brain related to multiple sclerosis,Alzheimer’s disease,Parkinson’s disease,vascular dementia,or chronic migrai

关键词： astrocytes brain glucagon-like peptide 1 receptor inflammation microglia

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Effect of SARS-CoV-2 infection on semenparameters in sperm bank volunteers with normalsperm concentration

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Asian Journal of Andrology 2024年第3期26卷 328-332页

作者： Li Wang Wen-Kai Han Xiao-Hui Song Qi-Lin Zhang An-Quan Guan Yuan Gao Jin-Long Ma Center for Reproductive Medicine Shandong UniversityJinan 250001China State key laboratory of Reproductive Medicine and Offspring Health ShandongUniversityJinan 250001China key laboratory of Reproductive endocrinology of Ministry of Education Shandong UniversityJinan 250001China Shandong keylaboratory of Reproductive Medicine Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityJinan 250001China Shandong Provincial ClinicalResearch Center for Reproductive Health Jinan 250001China Shandong Technology Innovation Center for Reproductive Health Jinan 250001China NationalResearch Center for Assisted Reproductive Technology and Reproductive Genetics Shandong UniversityJinan 250001China Research Unit of Gametogenesis andHealth of ART-Offspring Chinese Academy of Medical Sciences(No.2021RU001)Jinan 250001China.

In this study,we aimed to assess the effect of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection on semenparameters.The study comprised 110 sperm volunteers who self-reported SARS-CoV-2 infection from the Human Sperm Bank ofthe Center for Reproductive Medicine,Shandong University(Jinan,China).The volunteers had normal sperm concentration beforeinfection.Each volunteer provided semen samples before and after infection.We selected 90 days after infection as the cutoff point.Semen parameters within 90 days after infection of 109 volunteers(group A)were compared with semen parameters before infection.Moreover,semen parameters on or after 90 days after infection of 36 volunteers(group B)were compared with semen parameters beforeinfection.Furthermore,based on whether the volunteers had completed the three-dose SARS-CoV-2 vaccination booster,volunteersin group A and B were further divided into two subgroups separately.Semen parameters were compared before and after infection ineach subgroup.Our results showed that in this cohort population,the semen quality in volunteers with normal sperm concentrationsbefore infection decreased after SARS-CoV-2 infection within 90 days,while the semen quality returned to preinfection levels after 90days.The completion of a three-dose SARS-CoV-2 vaccination booster may exert a protective effect on semen quality after infection.

关键词： SARS-CoV-2 SARS-CoV-2 vaccination semen quality sperm donation sperm parameters

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