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Magnetic labeling of primary murine monocytes using very small superparamagnetic iron oxide nanoparticles

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Neural Regeneration Research 2022年第10期17卷 2311-2315页

作者： Martin Pohland Christoph Pohland Jürgen Kiwit Jana Glumm Institute of cell biology and Neurobiology Center for AnatomyCharité-Universitätsmedizin BerlinBerlinGermany Department of Neurosurgery Helios Klinikum Berlin BuchBerlinGermany

Due to their very small size,nanoparticles can interact with all cells in the central nervous *** of the most promising nanoparticle subgroups are very small superparamagnetic iron oxide nanoparticles(VSOP)that are citrate coated for electrostatic *** determine their influence on murine blood-derived monocytes,which easily enter the injured central nervous system,we applied VSOP and carboxydextran-coated superparamagnetic iron oxide nanoparticles(Resovist).We assessed their impact on the viability,cytokine,and chemokine secretion,as well as iron uptake of murine blood-derived *** found that(1)the monocytes accumulated VSOP and Resovist,(2)this uptake seemed to be nanoparticle-and time-dependent,(3)the decrease of monocytes viability was treatment-related,(4)VSOP and Resovist incubation did not alter cytokine homeostasis,and(5)overall a 6-hour treatment with 0.75 mM VSOP-R1 was probably sufficient to effectively label monocytes for future *** homeostasis is not altered,it is safe to label blood-derived monocles with *** labeled monocytes can be used to study injured central nervous system sites further,for example with drug-carrying VSOP.

关键词： CD11b,cytokine Ferucarbotran Mac1 MPS MRI Resovist superparamagnetic iron oxide nanoparticles(SPIO) very small superparamagnetic iron oxide nanoparticles(VSOP) viability

Monogenic diabetes in children:An underdiagnosed and poorly managed clinical dilemma

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World Journal of Diabetes 2024年第6期15卷 1051-1059页

作者： Saptarshi Bhattacharya Joseph M Pappachan Department of Endocrinology Indraprastha Apollo HospitalsDelhi 110076India Department of Endocrinology and Metabolism Lancashire Teaching Hospitals NHS TrustPreston PR29HTUnited Kingdom Faculty of Science Manchester Metropolitan UniversityManchester M156BHUnited Kingdom Faculty of biology Medicine and HealthThe University of ManchesterManchester M139PLUnited Kingdom

Monogenic diabetes,constituting 1%-2%of global diabetes cases,arises from single gene defects with distinctive inheritance *** over 50 associated genetic disorders,accurate diagnoses and management of monogenic diabetes remain inadequate,underscoring insufficient clinician *** disease spectrum encompasses maturity-onset diabetes of the young(MODY),characterized by distinct genetic mutations affecting insulin secretion,and neonatal diabetes mellitus(NDM)-a heterogeneous group of severe hyperglycemic disorders in *** diabetes,autoimmune monogenic diabetes,genetic insulin resistance and lipodystrophy syndromes further diversify the monogenic diabetes landscape.A tailored approach based on phenotypic and biochemical factors to identify candidates for genetic screening is recommended for suspected cases of *** diagnosis warrants immediate molecular genetic testing for infants under six *** these genetic defects presents a unique opportunity for precision *** research aimed to develop cost-effective genetic testing methods and gene-based therapy can facilitate appropriate identification and optimize clinical *** and study of new genes offer a valuable opportunity to gain deeper insights into pancreatic cell biology and the pathogenic mechanisms underlying common forms of *** clinical review published in the recent issue of World Journal of Diabetes is such an attempt to fill-in our knowledge gap about this enigmatic disease.

关键词： Monogenic diabetes Maturity-onset diabetes of the young Neonatal diabetes Mitochondrial diabetes Insulin resistance syndromes Genetic testing Next generation sequencing

Intermediate conductance, Ca^2＋-activated K^＋ channels： a novel target for chronic renal diseases

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Frontiers in biology 2015年第1期10卷 52-60页

作者： Claudia A. BERTUCCIO Daniel C. DEVOR Department of cell biology School of Medicine University of Pittsburgh Pittsburgh PA 15261 USA

Renal failure is a medical condition in which the kidneys are not working properly. There are two types of kidney failure： 1） acute kidney failure, which is sudden and often reversible with adequate treatment; and 2） chronic renal failure, which develops slowly and often is not reversible. The last stage of chronic renal failure is fatal without dialysis or kidney transplant. The treatment for chronic renal failure is focusing on slowing the progression of kidney damage. Several reports have described a promising approach to slow the loss of renal function through inhibition of the basolateral membrane, Ca^2＋-activated K^＋（KCa3.1） channel with a selective and nontoxic blocker TRAM-34. This review summarizes pathophysiological studies that describe the role of KCa3.1 in kidney diseases.

关键词： Ca^2+-activated K^+ channels KCa3.1 renal fibrosis polycystic kidney disease diabetes nephropathy transplant,cell proliferation C1 secretion renal failure

Role of glycosylation in TGF-β signaling and epithelial-to-mesenchymal transition in cancer

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Protein & cell 2021年第2期12卷 89-106页

作者： Jing Zhang Peter ten Dijke Manfred Wuhrer Tao Zhang Oncode Institute and cell Chemical biology Leiden University Medical Center2300 RC LeidenThe Netherlands Center for Proteomics and Metabolomics Leiden University Medical CenterLeidenThe Netherlands

Glycosylation is a common posttranslational modification on membrane-associated and secreted proteins that is of pivotal importance for regulating cell *** glycosylation can lead to uncontrolled cell proliferation,cell-matrix interactions,migration and differentiation,and has been shown to be involved in cancer and other *** epithelial-to-mesenchymal transition is a key step in the metastatic process by which cancer cells gain the ability to invade tissues and extravasate into the *** cellular transformation process,which is associated by morphological change,loss of epithelial traits and gain of mesenchymal markers,is triggered by the secreted cytokine transforming growth factor-β(TGF-β).TGF-βbioactivity is carefully regulated,and its effects on cells are mediated by its receptors on the cell *** this review,we first provide a brief overview of major types of glycans,namely,N-glycans,O-glycans,glycosphingolipids and glycosaminoglycans that are involved in cancer ***,we summarize studies on how the glycosylation of TGF-βsignaling components regulates TGF-βsecretion,bioavailability and TGF-βreceptor ***,we review glycosylation changes associated with TGF-β-induced epithelial-to-mesenchymal transition in *** and understanding the mechanisms by which glycosylation affects TGF-βsignaling and downstream biological responses will facilitate the identification of glycans as biomarkers and enable novel therapeutic approaches.

关键词： cancer epithelial-to-mesenchymal transition glycosphingolipids N-glycosylation Oglycosylation transforming growth factor-β

Autophagy mediates the secretion of macrophage migration inhibitory factor from cardiomyocytes upon serum-starvation

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Science China(Life Sciences) 2019年第8期62卷 1038-1046页

作者： Jimin Wu Xiangning Deng Juan Gao Wei Gao Han Xiao Xinyu Wang Youyi Zhang Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors Research

Macrophage migration inhibitory factor(MIF) is an inflammatory cytokine. It is elevated early in the blood of acute myocardial infarction patients. However, it is unclear whether and how MIF is released. This study investigated the cellular source and mechanism of MIF release from hearts. An ischemia-mimic treatment induced the secretion of MIF from neonatal rat cardiomyocytes but not from fibroblasts. The treatment did not cause significant leakage of lactate dehydrogenase, suggesting that ischemia induced the MIF secretion without causing severe cell damage. Plasma samples from patients with acute chest pain at the emergency department were collected for the detection of MIF. MIF levels in patients with acute coronary syndrome(ACS)increased early, when cardiac injury markers were not yet elevated, suggesting that ischemia can induce MIF secretion before the occurrence of severe myocardial damage. Serum-starvation caused MIF secretion from rat cardiomyocytes and Langendorffperfused rat hearts. The secretion was suppressed by the inhibition of autophagy by inhibitors or by silencing of Atg5. In conclusion, serum-starvation induces the secretion of MIF from cardiomyocytes via autophagy dependent pathway. Clarifying the mechanism of MIF secretion will be helpful for its application in the early diagnosis and treatment of ACS.

关键词： macrophage migration inhibitory factor cardiomyocyte ischemia autophagy secretion

Propofol inhibits cells migration and invasion via HOTAIR/miR-93/HIF-1α-mediated lactate secretion in colon cancer

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BIOcell 2021年第6期45卷 1585-1599页

作者： RUONAN GU WENJING GUO WENYANG WANG GUIHUAN LI XIAOJU LAI ZHIBIN HUANG WANLU ZHAO ZHICONGWU HUA CHEN WENYANG LUO FANGYIN ZENG FAN DENG Department of cell biology School of Basic Medical SciencesSouthern Medical UniversityGuangzhou510515China Department of Anesthesiology Zhujiang HospitalSouthern Medical UniversityGuangzhou510282China Department of Clinical laboratory The Fifth Affiliated HospitalSouthern Medical UniversityGuangzhou510920China

Propofol,a common intravenous anesthetic used in clinical,has been shown to regulate cells proliferation,inflammation,angiogenesis and metastasis as well as exerting anti-cancer effect in several different types of ***,the functions and mechanisms of propofol in lactate secretion and invasion of cancer cells remain *** primary aim of this study was to investigate the role of propofol in cells migration and invasion of colon cancer(CRC).Scratches assay,Transwell assay were used to detect colon cells migration and *** Quantitative Polymerase Chain Reaction(RT-qPCR),Western blotting were utilized to detect the expression of related ***-luciferase assay was performed to identify transcriptional activity of target genes,RNA pulldown assay was used to confirm the interactions of *** indicated that propofol inhibited cell migration and invasion through suppressing lactic acid production in ***,propofol reduced lactic acid production by down-regulating the expression of hypoxia inducible factor-1α(HIF-1α)and monocarboxylate transporter 4(MCT4).In addition,propofol inhibited the expression of HIF-1αand cells migration/invasion via suppressing the interaction of HOX transcript antisense RNA(HOTAIR)with *** present study indicated that propofol inhibited colon cancer cell migration and invasion by reducing lactic acid production and the expression of HIF-1αand MCT4 via HOTAIR/miR-93 *** data may provide potential metabolic targets for CRC treatment.

关键词： Propofol Colon cancer Lactic acid HIF-1α HOTAIR miR-93

MicroRNA-24 promotes pancreatic beta cells toward dedifferentiation to avoid endoplasmic reticulum stress-induced apoptosis

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Journal of Molecular cell biology 2019年第9期11卷 747-760页

作者： Yunxia Zhu Yi Sun Yuncai Zhou Yan Zhang Tao Zhang Yating Li Weiyan You Xiaoai Chang Li Yuan Xiao Han Key laboratory of Human Functional Genomics of Jiangsu Province Department of Biochemistry and Molecular BiologyNanjing Medical UniversityNanjing 210029China

Current research indicates that beta cell loss in type 2 diabetes may be attributed to beta cell dedifferentiation rather than apoptosis;however,the mechanisms by which this occurs remain poorly *** previous study demonstrated that elevation of microRNA-24(miR-24)in a diabetic setting caused beta cell dysfunction and replicative *** this study,we focused on the role of miR-24 in beta cell apoptosis and dedifferentiation under endoplasmic reticulum(ER)stress *** found that miR-24 overabundance protected beta cells from thapsigargin-induced apoptosis at the cost of accelerating the impairment of glucosestimulated insulin secretion(GSIS)and enhancing the presence of dedifferentiation ***?Pathway Analysis(IPA)revealed that elevation of miR-24 had an inhibitory effect on XBP1 and ATF4,which are downstream effectors of two key branches of ER stress,by inhibiting its direct target,***,elevated miR-24 initiated another pathway that targeted Mafa and decreased GSIS function in surviving beta cells,thus guiding their dedifferentiation under ER stress *** results demonstrated that the elevated miR-24,to the utmost extent,preserves beta cell mass by inhibiting apoptosis and inducing *** study not only provides a novel mechanism by which miR-24 dominates beta cell turnover under persistent metabolic stress but also offers a therapeutic consideration for treating diabetes by inducing dedifferentiated beta cells to re-differentiation.

关键词： microRNA-24 ER stress apoptosis dedifferentiation type 2 diabetes pancreatic beta cells

Endoplasmic reticulum targeted AIE bioprobe as a highly efficient inducer of immunogenic cell death

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Science China Chemistry 2020年第10期63卷 1428-1434页

作者： Jun Li Heqi Gao Ruihua Liu Chao Chen Sheng Zeng Qian Liu Dan Ding Key laboratory of Bioactive Materials Ministry of Education College of Life Sciencesand State Key Laboratory of Medicinal Chemical BiologyNankai UniversityTianjin 300071China Department of Urology Tianjin First Central HospitalTianjin 300192China

Focused oxidative stress of the specific organelles(e.g.,endoplasmic reticulum(ER)and mitochondrion)of cancer cells can boost the immunogenic cell death(ICD)effect for cancer ***,an ER-targeted bioprobe with aggregationinduced emission(AIE)characteristics(TPE-PR-FFKDEL)was rationally designed and synthesized by integrating a new AIE photosensitizer with ER targeting peptide,which has been demonstrated to be able to efficiently induce ER oxidative stress to evoke *** with the photosensitizer hypericin that is well-known as an ER-targeted ICD inducer,TPE-PR-FFKDEL can lead to more robust emission of immunostimulatory damage-associated molecular patterns such as surface-exposed calreticulin,ATP secretion,and high-mobility group protein B1(HMGB1)and heat shock protein 70(HSP 70)***,a range of immune responses are activated to protect mice from the attack of cancer cells in vivo.

关键词： immunogenic cell death endoplasmic reticulum oxidative stress aggregation-induced emission reactive oxygen species

EBV-Induced Human CD8^＋ NKT cells Synergise CD4^＋ NKT cells Suppressing EBV-Associated Tumours upon Induction of Thl-Bias

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cellular & Molecular Immunology 2009年第5期6卷 367-379页

作者： Wei Xiao Li Li Rui Zhou Ruijing Xiao Yujuan Wang Xiang Ji Mengjun Wu Lan Wang Wei Huang Xiaoling Zheng Xinti Tan Lang Chen Tao Xiong Jie Xiong Youxin Jin Jinquan Tan Yuling He laboratory of Allergy and Clinical Immunology Institute of Allergy andImmune-related Diseases Center for Medical Research and Department ofImmunology Wuhan University School of Medicine Wuhan China Section of Geriatrics Department of Internal Medicine the Renmin HospitalWuhan University Wuhan China The State Key laboratory of Molecular biology Institute of Biochemistryand Cell Biology Shanghai Institutes for Biological Sciences ChineseAcademy of Science Shanghai China These authors contributed equally to this work laboratory of Allergy and Clinical Immunology Institute of Allergy and Immune-related Diseases Center for Medical Research and Department of Immunology Wuhan University School of Medicine Dong Hu Road 185 Wuchang 430071 Wuhan China

CD8^＋ natural killer T （NKT） cells from EBV-associated tumour patients are quantitatively and functionally impaired. EBV-induced CD8^＋ NKT cells drive syngeneic T cells into a Thl-bias response to suppress EBV-associated malignancies. IL-4-biased CD4^＋ NKT cells do not affect either syngeneic T cell cytotoxicity or Th cytokine secretion. Circulating mDC1 cells from patients with EBV-associated malignancies impair the production of IFN-T by CD8^＋ NKT cells. In this study, we have established a human-thymus-SCID chimaera model to further investigate the underlying mechanism of EBV-induced CD8^＋ NKT cells in suppressing EBV-associated malignancies. In the human-thymus-SCID chimera, EBV-induced CD8^＋ NKT cells suppress EBV-associated malignancies in a manner dependent on the Thl-bias response and syngeneic CD3^＋ T cells. However, adoptive transfer with CD4^＋ NKT cells alone inhibits T cell immunity. Interestingly, CD4^＋ NKT cells themselves secrete high levels of IL-2, enhancing the persistence of adoptively transferred CD8^＋ NKT cells and T cells, thereby leading to a more pronounced T cell anti-tumour response in chimaeras co-transferred with CD4^＋ and CD8^＋ NKT cells. Thus, immune reconstitution with EBV-induced CD4^＋ and CD8^＋ NKT cells synergistically enhances T cell tumour immunity, providing a potential prophylactic and therapeutic treatment for EBV-associated malignancies.

关键词： CD8^+ NKT cells EBV human-thymus-SCID chimaeras IFN-γ