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ATP6AP2,a regulator of LRP6/β-catenin protein trafficking,promotes Wnt/β-catenin signaling and bone formation in a cell type dependent manner

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Bone Research 2024年第2期12卷 453-468页

作者： Lei Xiong Hao-Han Guo Jin-Xiu Pan Xiao Ren Daehoon Lee Li Chen Lin Mei Wen-Cheng Xiong Department of Neurosciences School of MedicineCase Western Reserve UniversityClevelandOH 44106USA Louis Stoke VA medical center ClevelandOH 44106USA

Wnt/β-catenin signaling is critical for various cellular processes in multiple cell types,including osteoblast(OB)differentiation and *** how Wnt/β-catenin signaling is regulated in OBs remain ***6AP2,an accessory subunit of V-ATPase,plays important roles in multiple cell types/organs and multiple signaling ***,little is known whether and how ATP6AP2 in OBs regulates Wnt/β-catenin signaling and bone *** we provide evidence for ATP6AP2 in the OB-lineage cells to promote OB-mediated bone formation and bone homeostasis selectively in the trabecular bone *** knocking out(CKO)ATP6AP2 in the OB-lineage cells(Atp6ap2^(Ocn-Cre))reduced trabecular,but not cortical,bone formation and bone *** and cellular biochemical studies revealed that LRP6 and N-cadherin were reduced in ATP6AP2-KO BMSCs and OBs,but not *** in vitro and in vivo studies revealed impairedβ-catenin signaling in ATP6AP2-KO BMSCs and OBs,but not osteocytes,under both basal and Wnt stimulated conditions,although LRP5 was decreased in ATP6AP2-KO osteocytes,but not *** cell biological studies uncovered that osteoblastic ATP6AP2 is not required for Wnt3a suppression ofβ-catenin phosphorylation,but necessary for LRP6/β-catenin and N-cadherin/β-catenin protein complex distribution at the cell membrane,thus preventing their *** of activeβ-catenin diminished the OB differentiation deficit in ATP6AP2-KO *** together,these results support the view for ATP6AP2 as a critical regulator of both LRP6 and N-cadherin protein trafficking and stability,and thus regulatingβ-catenin levels,demonstrating an un-recognized function of osteoblastic ATP6AP2 in promoting Wnt/LRP6/β-catenin signaling and trabecular bone formation.

关键词： LRP6 impaired organs

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Predicting hepatocellular carcinoma: A new non-invasive model based on shear wave elastography

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World Journal of Gastroenterology 2024年第25期30卷 3166-3178页

作者： Dong Jiang Yi Qian Yi-Jun Gu Ru Wang Hua Yu Hui Dong Dong-Yu Chen Yan Chen Hao-Zheng Jiang Bi-Bo Tan Min Peng Yi-Ran Li Department of Ultrasound Eastern Hepatobiliary Surgery HospitalThe Third Affiliated Hospital of Naval Medical UniversityShanghai 200433China Department of Pathology Shanghai Eastern Hepatobiliary Surgery HospitalThird Affiliated Hospital of Naval Medical UniversityShanghai 200433China Department of College of Art and Science Case Western Reserve UniversityClevelandOH 44106United States Ultrasound Diagnosis PLA Naval Medical CenterShanghai 200437China

BACKGROUND Integrating conventional ultrasound features with 2D shear wave elastography(2D-SWE)can potentially enhance preoperative hepatocellular carcinoma(HCC)*** To develop a 2D-SWE-based predictive model for preoperative identification of *** A retrospective analysis of 884 patients who underwent liver resection and pathology evaluation from February 2021 to August 2023 was conducted at the Oriental Hepatobiliary Surgery *** patients were divided into the modeling group(n=720)and the control group(n=164).The study included conventional ultrasound,2D-SWE,and preoperative laboratory *** logistic regression was used to identify independent predictive factors for RESULTS In the modeling group analysis,maximal elasticity(Emax)of tumors and their peripheries,platelet count,cirrhosis,and blood flow were independent risk indicators for *** factors yielded an area under the curve of 0.77(95%confidence interval:0.73-0.81)with 84%sensitivity and 61%*** model demonstrated good calibration in both the construction and validation cohorts,as shown by the calibration graph and Hosmer-Lemeshow test(P=0.683 and P=0.658,respectively).Additionally,the mean elasticity(Emean)of the tumor periphery was identified as a risk factor for microvascular invasion(MVI)in malignant liver tumors(P=0.003).Patients receiving antiviral treatment differed significantly in platelet count(P=0.002),Emax of tumors(P=0.033),Emean of tumors(P=0.042),Emax at tumor periphery(P<0.001),and Emean at tumor periphery(P=0.003).CONCLUSION 2D-SWE’s hardness value serves as a valuable marker for enhancing the preoperative diagnosis of malignant liver lesions,correlating significantly with MVI and antiviral treatment efficacy.

关键词： Shear wave elastography Predicting model Microvascular invasion Antiviral treatment Hepatocellular carcinoma

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Monogenic deficiency in murine intestinal Cdc42 leads to mucosal inflammation that induces crypt dysplasia

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Genes & Diseases 2024年第1期11卷 413-429页

作者： Dongsheng Zhang Wenjuan Tang Haitao Niu William Tse Hai-Bin Ruan Helmut Dolznig Thomas Knosel Friedrich Karl-Heinz Madeleine Themanns Jiang Wang Mingquan Song Lee Denson Lukas Kenner Richard Moriggl Yi Zheng Xiaonan Han Division of Hematology and Oncology Division of Cancer BiologyDepartment of MedicineMetroHealth Medical Center(MHMC)Case Western Reserve University(CWRU)School of MedicineClevelandOH 44109USA Cancer Genomics and Epigenomics Program Case Comprehensive Cancer CenterCase Western Reserve University(CWRU)ClevelandOH 44106USA Division of Gastroenterology Hepatology and NutritionCincinnati Children’s Hospital Medical Center(CCHMC)CincinnatiOH 45229USA Children’s Hospital of Fudan university Shanghai 201102China School of Medicine Jinan UniversityGuangzhouGuangdong 510632China Laboratory Animal Science(ILAS) Chinese Academy of Medical Science(CAMS)and Peking Union Medical College(PUMC)Beijing 100006China Department of Integrative Biology and Physiology University of Minnesota Medical SchoolMinneapolisMI 55455USA Institute of medical Genetics Medical University of ViennaVienna 1040Austria Institute of Pathology Ludwig-Maximilians-University MunichMunich 80539Germany Institute of Biochemistry II University Hospital JenaJena 07743Germany Laboratory Animal Pathology University of Veterinary Medicine ViennaVienna 1210Austria Department of Pathology University of CincinnatiCincinnatiOH 45221USA Department of Gastroenterology The Affiliated Hospital of Qingdao UniversityQingdaoShandong 266005China Department of Pathology Medical University of ViennaVienna 1040Austria Ludwig Boltzmann Institute for Cancer Research Vienna 1090Austria medical university of Vienna Vienna 1040Austria Institute of Animal Breeding and Genetics University of Veterinary Medicine ViennaVienna 1210Austria Division of Experimental Hematology CCHMCCincinnatiOH 45229USA

CDC42 controls intestinal epithelial(IEC)stem cell(IESC)*** aberrant CDC42 initiates intestinal inflammation or neoplasia is *** utilized models of inflam-matory bowel diseases(IBD),colorectal cancer,aging,and IESC injury to determine the loss of intestinal Cdc42 upon inflammation and *** specimens were collected to determine the levels of CDC42 in IBD or colorectal ***42 floxed mice were crossed with Villin-Cre,Villin-CreERT2 and/or Lgr5-eGFP-IRES-CreERT2,or Bmi1-CreERT2 mice to generate Cdc42 deficient ***,colitis,aging,and intestinal organoid were used to evaluate CDC42 upon mucosal inflammation,IESC/progenitor regenerative capacity,and IEC *** studies revealed that increased CDC42 in colorectal cancer correlated with lower survival;in contrast,lower levels of CDC42 were found in the inflamed IBD *** Cdc42 depletion significantly reduced Lgr5+IEsCs,increased progenitors'hyperplasia,and induced mucosal inflammation,which led to crypt *** Cdc42 depletion markedly enhanced irra-diation-or chemical-induced *** or inhibition of Cdc42 reduced colonic Lgr5+IESC *** conclusion,depletion of Cdc42 reduces the IESC regeneration and IEC repair,leading to prolonged mucosal *** monogenic loss of Cdc42 in-duces mucosal inflammation,which could result in intestinal neoplasia in the context of aging.

关键词： Cell divisioncycle 42(CDC42) Colitis Colorectal cancer(CRC) Inflammatory bowel diseases(IBD) Intestinal epithelial cell(IEC) Intestinal epithelial stem cell(IESC) Irradiation

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Ferroptosis in chronic obstructive pulmonary disease:From cellular mechanisms to therapeutic applications

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Chinese medical Journal 2024年第10期137卷 1237-1239页

作者： Mengli Yan Shiyu Xu Han Wang Shoujin Dong Chunheng Mo The Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE State Key Laboratory of BiotherapyWest China Second University HospitalSichuan UniversityChengduSichuan 610041China Department of Nephrology Henan Provincial Clinical Research Center for Kidney DiseaseHenan Provincial Key Laboratory of Kidney Disease and ImmunologyHenan Provincial People’s Hospital and People’s Hospital of Zhengzhou UniversityZhengzhouHenan 450000China Department of Biochemistry School of MedicineCase Western Reserve UniversityClevelandOH 44106USA center for RNA Science and Therapeutics School of MedicineCase Western Reserve UniversityClevelandOH 44106USA Department of Pulmonary and Critical Care Medicine Chengdu First People’s HospitalChengduSichuan 610095China

To the Editor:Chronic obstructive pulmonary disease(COPD)is a global public health challenge without effective treatment currently available,affecting>300 million individuals *** understanding the pathogenesis of this disease is ***,ferroptosis,a form of cell death driven by iron-dependent lipid peroxidation,has been associated with the pathogenesis of COPD.[1]Multiple signaling pathways,such as glutathione peroxidase 4(GPX4),ferroptosis suppressor protein 1(FSP1),and tetrahydrobiopterin-dependent pathways,as well as iron metabolism,are involved in regulating ferroptosis[2,3][Figure 1A].Here,we provide a comprehensive overview of recent advances in understanding the role of ferroptosis in COPD,highlighting potential therapeutic strategies targeting ferroptosis for treating the disease.

关键词： therapeutic metabolism peroxidation

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Brain-wide activation involved in 15 mA transcranial alternating current stimulation in patients with first-episode major depressive disorder

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General Psychiatry 2024年第2期37卷 265-273页

作者： Jie Wang Wenfeng Zhao Huang Wang Haixia Leng Qing Xue Mao Peng Baoquan Min Xiukun Jin Liucen Tan Keming Gao Hongxing Wang Songjiang Hospital and Songjiang Research Institute Shanghai Key Laboratory of Emotions and Affective DisordersShanghai Jiao Tong University School of MedicineShanghaiChina Institute of Neuroscience and Brain Diseases Xiangyang Central HospitalAffiliated Hospital of Hubei University of Arts and ScienceXiangyangHubeiChina Division of Neuropsychiatry and Psychosomatics Department of NeurologyXuanwu Hospital of Capital Medical UniversityBeijingChina Electroconvulsive Therapy University Hospitals Cleveland Medical CenterClevelandOhioUSA Department of Psychiatry Case Western Reserve University School of MedicineClevelandOhioUSA Institute of Sleep and Consciousness Disorders Center of EpilepsyBeijing Institute for Brain DisordersCapital Medical UniversityBeijingChina Institute of Special medical Sciences School of Forensic MedicineShanxi Medical UniversityTaiyuanShanxiChina

Background Although 15 mA transcranial alternating current stimulation(tACS)has a therapeutic effect on depression,the activations of brain structures in humans accounting for this tACS configuration remain largely *** To investigate which intracranial brain structures are engaged in the tACS at 77.5 Hz and 15 mA,delivered via the forehead and the mastoid electrodes in the human *** Actual human head models were built using the magnetic resonance imagings of eight outpatient volunteers with drug-naïve,first-episode major depressive disorder and then used to perform the electric field distributions with SimNIBS *** The electric field distributions of the sagittal,coronal and axial planes showed that the bilateral frontal lobes,bilateral temporal lobes,hippocampus,cingulate,hypothalamus,thalamus,amygdala,cerebellum and brainstem were visibly stimulated by the 15 mA tACS *** Brain-wide activation,including the cortex,subcortical structures,cerebellum and brainstem,is involved in the 15 mA tACS intervention for first-episode major depressive *** results indicate that the simultaneous involvement of multiple brain regions is a possible mechanism for its effectiveness in reducing depressive symptoms.

关键词： stimulation involvement activation

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Pien Tze Huang Inhibits Proliferation of Colorectal Cancer Cells through Suppressing PNO1 Expression and Activating p53/p21 Signaling Pathway

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Chinese Journal of Integrative Medicine 2024年第6期30卷 515-524页

作者： CAO Liu-jing LIU Li-ya CHEN You-qin HAN Yu-ying WEI Li-hui YAO Meng-ying FANG Yi WU Mei-zhu CHENG Ying Thomas J.Sferra LIU Hui-xin LI Li PENG Jun SHEN A-ling Clinical Research Institute the Second Affiliated Hospital&Academy of Integrative MedicineFujian University of Traditional Chinese MedicineFuzhou350122China Fujian Key Laboratory of Integrative Medicine in Geriatrics Fujian University of Traditional Chinese MedicineFuzhou350122China Department of Pediatrics Case Western Reserve University School of MedicineUH Rainbow Babies and Children’s HospitalClevelandOH44106USA Innovation and Transformation center Fujian University of Traditional Chinese MedicineFuzhou350122China Department of Health Management Fujian Provincial HospitalShengli Clinical College of Fujian Medical UniversityFuzhou000000China

ObjectiveTo explore the regulatory effect of Pien Tze Huang (PZH) on targeting partner of NOB1 (PNO1) and it’s down-stream mediators in colorectal cancer (CRC) *** polymerase chain reaction was performed to determine mRNA levels of PNO1, TP53, and CDKN1A. western blotting was performed to determine protein levels of PNO1, p53, and p21. HCT-8 cells were transduced with a lentivirus over-expressing PNO1. Colony formation assay was used to detect cell survival in PNO1 overexpression of HCT-8 cells after PZH treatment. Cell-cycle distribution, cell viability and cell apoptosis were performed to identify the effect of PNO1 overexpression on cell proliferation and apoptosis of HCT-8 cells after PZH treatment. Xenograft BALB/c nude mice bearing HCT116 cells transduced with sh-PNO1 or sh-Ctrl lentivirus were evaluated. western blot assay was performed to detect PNO1, p53, p21 and PCNA expression in tumor sections. Terminal deoxynucleotidyl transferase dUTP nick end labling (TUNEL) assay was used to determine the apoptotic cells in *** treatment decreased cell viability, down-regulated PNO1 expression, and up-regulated p53 and p21 expressions in HCT-8 cells (P<0.05). PNO1 overexpression attenuated the effects of PZH treatment, including the expression of p53 and p21, cell growth, cell viability, cell cycle arrest and cell apoptosis in vitro (P<0.05). PNO1 knockdown eliminated the effects of PZH treatment on tumor growth, inhibiting cell proliferation inhibition and apoptosis induction in vivo (P<0.05). Similarly, PNO1 knockdown attenuated the effects of PZH treatment on the down-regulation of PNO1 and up-regulation of p53 and p21 in vivo (P<0.05).ConclusionThe mechanism by which PZH induces its CRC anti-proliferative effect is at least in part by regulating the expression of PNO1 and its downstream targets p53 and p21.

关键词： colorectal cancer Pien Tze Huang Chinese medicine partner of NOB1 proliferation p53/p21 pathway

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Multidisciplinary management of ulcerative colitis complicated by immune checkpoint inhibitor-associated colitis with life-threatening gastrointestinal hemorrhage:A case report

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World Journal of Gastrointestinal Surgery 2024年第7期16卷 2329-2336页

作者： Na Hong Bo Wang Hang-Cheng Zhou Zheng-Xiang Wu Hua-Ying Fang Geng-Qing Song Yue Yu Department of Gastroenterology The First Affiliated Hospital of University of Science and Technology of ChinaDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230001Anhui ProvinceChina Department of Pathology The First Affiliated Hospital of University of Science and Technology of ChinaDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230036Anhui ProvinceChina Intelligent Pathology Institute Division of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230036Anhui ProvinceChina Department of Gastroenterology and Hepatology Metro Health Medical CenterCase Western Reserve UniversityClevelandOH 44109United States

BACKGROUND Programmed cell death 1(PD-1)inhibitors are immune checkpoint inhibitors(ICI)that have demonstrated significant efficacy in treating various advanced malignant *** most patients tolerate treatment well,several adverse drug reactions,such as fatigue,myelosuppression,and ICI-associated colitis,have been *** SUMMARY This case involved a 57-year-old male patient with ulcerative colitis complicated by hepatocarcinoma who underwent treatment with tirelizumab(a PD-1 inhibitor)for six *** treatment led to repeated life-threatening lower gastrointestinal *** patient received infliximab,vedolizumab,and other salvage procedures but ultimately required subtotal colectomy due to uncontrollable massive lower gastrointestinal ***,postoperative gastrointestinal bleeding has stopped,the patient’s stool has turned yellow,and his full blood cell count has returned to *** This case highlights the necessity of early identification,timely and adequate treatment of ICI-related colitis,and rapid escalation to achieve the goal of improving prognosis.

关键词： Ulcerative colitis Hepatocarcinoma Immune checkpoint inhibitor-associated colitis Colectomy case report

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Sam68 is a regulator of Toll-like receptor signaling

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Cellular & Molecular Immunology 2017年第1期14卷 107-117页

作者： Jeffrey A Tomalka Tristan J de Jesus Parameswaran Ramakrishnan Department of Pathology School of Medicine Case Western Reserve University and University Hospitals Case Medical Center Cleveland OH 44106 USA

Recognition of pathogens by Toll-like receptors （TLR） activate multiple signaling cascades and expression of genes tailored to mount a primary immune response, inflammation, cell survival and apoptosis. Although TLR-induced activation of pathways, such as nuclear factor kappaB （NF-κB） and mitogen-activated protein kinases （MAPK）, has been well studied, molecular entities controlling quantitative regulation of these pathways during an immune response remain poorly defined. We identified Sam68 as a novel regulator of TLR-induced NF-κB and MAPK activation. We found that TLR2 and TLR3 are totally dependent, whereas TLR4 is only partially dependent on Sam68 to induce the activation of NF-KB c-Rel. Absence of Sam68 greatly decreased TLR2- and TLR3-induced NF-κB p65 activation, whereas TLR4- induced p65 activation in a Sam68-independent manner. In contrast, Sam68 appeared to be a negative regulator of MAPK pathways because absence of Sam68 enhanced TLR2-induced activation of extracellular signal-regulated kinases （ERK） and c-Jun N-terminal kinases （JNK）. Interestingly, TLR2- and TLR3-induced gene expression showed a differential requirement of Sam68. Absence of Sam68 impaired TLR2-induced gene expression, suggesting that Sam68 has a critical role in myeloid differentiation primary response gene 88-dependent TLR2 signaling. TLR3-induced gene expression that utilize Toll/Interleukin-1 receptor-domain-containing adapter-inducing beta interferon pathway, depend only partially on Sam68. Our findings suggest that Sam68 may function as an immune rheostat that balances the activation of NF-κB p65 and c-Rel, as well as MAPK, revealing a potential novel target to manipulate TLR signaling.

关键词： innate immunity MAP kinase NF-kappaB Sam68 TLR

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Diabetic bladder dysfunction

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Chinese medical Journal 2014年第7期127卷 1357-1364页

作者： Guiming Liu Firouz Daneshgari Urology Institute University Hospitals Case Medical Center and Department of Urology Case Western Reserve University School of Medicine Cleveland Ohio USA

Objective To review studies on diabetic bladder dysfunction （DBD）,a common and bothersome complication of diabetes *** sources We performed a search of the English literature through *** key words used were ＂diabetes＂ and ＂bladder dysfunction＂ or ＂cystopathy＂.Our own data and perspective are included in the *** selection Studies containing data relevant to DBD were *** of the limited length of this article,we also referenced reviews that contain comprehensive amalgamations of relevant *** The classic symptoms of DBD are decreased bladder sensation,increased bladder capacity,and impaired bladder emptying with resultant elevated post-void residual ***,recent clinical and experimental evidence indicate a strong presence of storage problems such as urge incontinence in *** studies of DBD in animal models of type 1 diabetes have revealed temporal effects of diabetes,causing an early phase of compensatory bladder function and a later phase of decompensated bladder *** pathophysiology of DBD is multifactorial,including disturbances of the detrusor,urothelium,autonomic nerves,and *** and hyperglycemia play important but distinctive roles in induction of bladder dysfunction in type 1 *** causes significant bladder hypertrophy in the early stage of diabetes,whereas oxidative stress in the bladder caused by chronic hyperglycemia may play an important role in the late stage failure of bladder *** DBD includes time-dependent and mixed *** pathological alterations include muscle,nerve,and *** and hyperglycemia independently contribute to the pathogenesis of *** for DBD are *** clinical studies on DBD in type 1 and type 2 diabetes should be investigated *** studies of DBD in type 2 diabetes are needed,from the natural history to *** understanding of the molecular mechan

关键词： diabetes bladder dysfunction cystopathy complications

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Effect of Recql5 deficiency on the intestinal tumor susceptibility of Apc^(min) mice

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World Journal of Gastroenterology 2010年第12期16卷 1482-1486页

作者： Yiduo Hu,Xincheng Lu,Guangbin Luo,Department of Genetics,case Comprehensive Cancer center and university hospitals of Cleveland,case western reserve university,Cleveland,OH 44106,United States Yiduo Hu,Department of Cancer Biology,Dana-Farber Cancer Institute,Boston,MA 02115,United States Department of Genetics Case Comprehensive Cancer Center and University Hospitals of Cleveland Case Western Reserve University Cleveland OH 44106 USA

AIM:To investigate whether Recql5,a DNA helicase that plays an important role in the maintenance of genome integrity,is a tumor suppressor in the gastrointestinal tract in ***:We generated cohorts of both Recql5-proficient and Recql5-deficient Apcmin/+mice and compared the tumor susceptibility in their gastrointestinal ***:Recql5 deficiency in Apcmin/+mice resulted in a significant increase in the tumor incidence in both the colon(P=0.0162)and the small intestine(P<0.01).These findings have provided the first genetic evidence for a tumor suppression role of Recql5 in the gastrointestinal tract of ***,since mouse Recql5 and human RECQL5 are highly conserved,these findings also suggest that RECQL5 may be a tu-mor suppressor for human colon ***:Recql5 has a tumor suppression role in the mouse gastrointestinal tract.

关键词： Recql5 Apc Tumor suppressor Genome instability Colon cancer Apcmin/+mice

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