377 results on '"Guangjun Nie"'
Search Results
352. Review of Synthesis and Biomedical Applications of Typical Fluorescent Nanomaterials
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Tianjiao Ji, Xiao Yang, Guangjun Nie, Xixi Liu, and Wei Jingyan
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Materials science ,Applied Mathematics ,General Mathematics ,Nanotechnology ,Fluorescence ,Nanomaterials - Published
- 2013
353. Hydroxyethyl-functionalized ultrasmall chitosan nanoparticles as a gene delivery carrier
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Yanli Gao, Qianfen Zhuang, Libo Du, Yang Liu, Yanchao Li, Guangjun Nie, Hui Yang, and Hongying Jia
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Polyethylenimine ,Chemistry ,General Chemical Engineering ,Vesicle ,technology, industry, and agriculture ,General Chemistry ,Transfection ,Endocytosis ,Molecular biology ,Polyelectrolyte ,In vitro ,chemistry.chemical_compound ,In vivo ,Biophysics ,Cytotoxicity - Abstract
A non-viral gene vector based on hydroxyethyl ultra-low molecular weight chitosan nanoparticles (HE-ULMWCh NPs) has been synthesized. The HE-ULMWCh is used to form nanoparticles with an enhanced green fluorescence protein (pEGFP) encoding plasmid that possesses diameters of 30–50 nm and a molecular weight of less than 2 kDa. The cytotoxicity assay shows that this new gene vector is significantly less cytotoxic than polyethylenimine whilst still retaining the characteristics of a cationic polyelectrolyte. Cellular uptake of HE-ULMWCh NP–pDNA nanocomplexes shows that HE-ULMWCh NPs can readily enter into cells via endocytosis and then be delivered to lysosomes. pDNA can be easily released from HE-ULMWCh NPs in the acidic vesicles of lysosomes, therefore resulting in a significant increase in the transfection efficiency in three different cell lines compared to naked pDNA. The in vitro results using the new gene vector are further confirmed by in vivo transfection in which HE-ULMWCh NPs provided 3.2 fold greater transfection efficiency than naked pDNA. The HE-ULMWCh NPs can therefore be concluded to be a promising delivery system for in vitro and in vivo gene transfection.
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- 2013
354. Deciphering an Underlying Mechanism of Differential Cellular Effects of Nanoparticles: An Example of Bach-1 Dependent Induction of HO-1 Expression by Gold Nanorod
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Xiaochun Wu, Jingyan Wei, Xiao Yang, Yiye Li, Suping Li, Guangjun Nie, Zhenlin Fan, and Shiwen Niu
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Chemistry(all) ,Cell Survival ,Cell ,Gene Expression ,General Physics and Astronomy ,Nanoparticle ,Nanotechnology ,Physics and Astronomy(all) ,General Biochemistry, Genetics and Molecular Biology ,Cell Line ,Polyethylene Glycols ,Biomaterials ,Mice ,Materials Science(all) ,medicine ,Animals ,Humans ,General Materials Science ,Transcription factor ,Nanotubes ,Biochemistry, Genetics and Molecular Biology(all) ,Chemistry ,Mechanism (biology) ,General Chemistry ,Fibroblasts ,In vitro ,Quaternary Ammonium Compounds ,medicine.anatomical_structure ,Cell culture ,Colloidal gold ,Biophysics ,Polystyrenes ,Nanorod ,Gold ,Polyethylenes ,Heme Oxygenase-1 - Abstract
Gold nanoparticles are extensively investigated for their potential biomedical applications. Therefore, it is pertinent to thoroughly evaluate their biological effects at different levels and their underlying molecular mechanism. Frequently, there are discrepancies about the biological effects of various gold nanoparticles among the reports dealing with different models. Most of the studies focused on the different biological effects of various nano-properties of the nanomaterials. We hypothesize that the biological models with different metabolic processes would be taken into account to explain the observed discrepancies of biological effects of nanomaterials. Herein, by using mouse embryo fibroblast cell line (MEF-1) and human embryonal lung fibroblast cell line (MRC-5) as in vitro models, we studied the cellular effects of gold nanorods (AuNRs) coated with poly (diallyldimethyl ammonium chloride) (PDDAC), polyethylene glycol and polystyrene sulfonae (PSS). We found that all three AuNRs had no effects on cellular viability at the concentration of 1 nM; however, AuNRs that coated with PDDAC and PSS induced significant up-regulation of heme oxygenase-1 (HO-1) which was believed to be involved in cellular defense activities in MEF-1 but not in MRC-5 cells. Further study showed that the low fundamental expression of transcription factor Bach-1, the major regulator of HO-1 expression, in MEF-1 was responsible for the up-regulation of HO-1 induced by the AuNRs. Our results indicate that although AuNRs we used are non-cytotoxic, they cell-specifically induce change of gene expression, such as HO-1. Our current study provides a good example to explain the molecular mechanisms of differential biological effects of nanomaterials in different cellular models. This finding raises a concern on evaluation of cellular effects of nanoparticles where the cell models should be critically considered.
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- 2012
355. Graphene: Unraveling Stress-Induced Toxicity Properties of Graphene Oxide and the Underlying Mechanism (Adv. Mater. 39/2012)
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Xingfa Gao, Jun-Jie Yin, Yiye Li, Ying Fang, Chi Wang, Guangjun Nie, Zhongjun Li, Yu-Ting Zhou, Wendi Zhang, Yuliang Zhao, and Zhenzhen Lu
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Materials science ,Graphene ,Mechanical Engineering ,Stress induced ,Oxide ,Nanotechnology ,law.invention ,chemistry.chemical_compound ,Electron transfer ,chemistry ,Mechanics of Materials ,Nanotoxicology ,law ,Toxicity ,General Materials Science ,Mechanism (sociology) - Published
- 2012
356. Cellular Responses to Nanomaterials: Exosomes as Extrapulmonary Signaling Conveyors for Nanoparticle-Induced Systemic Immune Activation (Small 3/2012)
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Guangjun Nie, Yuliang Zhao, Weiyue Feng, Motao Zhu, Jian Shi, and Yiye Li
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Biomaterials ,Nanoparticle ,General Materials Science ,General Chemistry ,Biology ,Signal transduction ,Microvesicles ,Biotechnology ,Immune activation ,Cell biology ,Nanomaterials - Published
- 2012
357. Progress on Hepatic Oxidative Damage Mediated by Iron Homeostasis Disregulation and Other Detrimental Factors and Antioxidative Protection Strategy
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Ailian DONG, Yulin HU, Yabin QI, and Guangjun NIE
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Applied Mathematics ,General Mathematics - Published
- 2012
358. Enhancing photocatalytic activity of one-dimensional KNbO3 nanowires by Au nanoparticles under ultraviolet and visible-light
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Linjie Zhi, Xuemei Zhou, Jingchang Zhang, Guangjun Nie, Jiaguo Yu, Jinyao Lan, and Gang Liu
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Potassium niobate ,Materials science ,Nanowire ,Nanoparticle ,Nanotechnology ,Photochemistry ,chemistry.chemical_compound ,chemistry ,Photocatalysis ,Rhodamine B ,General Materials Science ,Nanorod ,Surface plasmon resonance ,Visible spectrum - Abstract
A novel photocatalyst was prepared by anchoring Au nanoparticles (NPs) onto one-dimensional potassium niobate (KNbO3) nanowires. Photocatalytic activity towards rhodamine B degradation over Au/KNbO3 appears to be much greater than that of KNbO3 nanowires, nanorods and commercial Alfa Aesar. In terms of reaction rate constant (k), ultraviolet excitation (λ = 365 nm) is higher than that of visible-light (λ > 420 nm) and increasing the size of Au NPs from 5 to 10 nm significantly improves the reactivity. Notably, Au NPs with a size of ca. 10 nm supported on KNbO3 nanowires display the greatest photoreactivity, with k exceeding that of commercial KNbO3 by a factor of 15. The mechanism responsible for the enhancement of photocatalytic activity was discussed, highlighting the crucial role of surface plasmon resonance as well as interband transitions on Au NPs. This study is potentially applicable to a range of low-dimensional niobate-based nanostructures combined with Au and other plasmonic NPs with promising applications in photocatalysis and relevant areas.
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- 2011
359. TfR1 and Ferrochelatase Expression During Erythroid Differentiation Induced by 5-Aza-Cdr In Both MEL Cells and BFU-E-Derived Erythroblasts Correlates with c-Myc Function
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Guangjun Nie, Gang Liu, Bo Ning, and Greg J. Anderson
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Regulation of gene expression ,Cellular differentiation ,Immunology ,Bisulfite sequencing ,Transferrin receptor ,Cell Biology ,Hematology ,Methylation ,Biology ,Ferrochelatase ,Biochemistry ,Molecular biology ,Gene expression ,biology.protein ,Transcription factor - Abstract
Abstract 4248 During erythroid differentiation, heme biosynthesis increases dramatically and this is accompanied by a marked increase in transferrin receptor 1 (TfR1) expression and iron uptake from transferrin. It has long been known that 5-aza-2′deoxycytidine (5-aza-CdR), a demethylating agent, is able to induce murine erythroid leukemia (MEL) cell differentiation. However, the detailed mechanism underlying this induction remains elusive. In the current study, we report that 5-aza-CdR induces erythroid differentiation in MEL cells and BFU-E-derived erythroblasts and that this is associated with the nuclear translocation of the transcription factor c-Myc and its binding to Max to form functional complex. As markers of erythroid differentiation, the expression levels of TfR1, ferrochelatase and ALAS2 were analyzed by quantitative real-time PCR and western blotting. TfR1 and ferrochelatase expression were increased 5-fold following 5-aza-CdR treatment. To determine whether these changes in gene expression reflected differential methylation, we analyzed 1.5 kb up- and downstream from the transcription start site (TS) of these genes. Although many potential methylation sites (CpG islands) were found in both the TfR1 and ferrochelatase genes, bisulfite sequencing revealed that few sites (< 5%) were methylated in these promoters in untreated MEL cells and that there was no difference following 5-aza-CdR treatment. This observation suggests that the increased expression of TfR1 and ferrochelatase is not directly mediated by 5-aza-CdR-induced DNA demethylation. EKLF and GATA1 are key transcription regulators in erythroid differentiation, and the iron regulatory proteins (IRPs) are important for the post-transcriptional regulation of TfR1 mRNA levels. Bioinformatic analysis showed that there were many potential methylation sites in the EKLF and IRP2 promoters, however, bisulfite sequencing showed that there was no effect of 5-aza-CdR treatment at these sites in MEL cells. Since c-Myc has been reported to stimulate TfR1 expression, we then investigated the role of c-Myc in erythroid differentiation. Levels of c-Myc mRNA and protein were not increased by 5-aza-CdR, however, we did observe a dramatic increase in the nuclear fraction of c-Myc. Furthermore, co-immunopricipitation studies showed that the amount of the Myc-Max complex, which is the form in which c-Myc activates downstream gene expression, increased in the nucleus after 5-aza-CdR treatment. Interestingly, using chromatin-immunoprecipitation we also observed very strong binding of c-Myc to the CACGTG sequence upstream of the TfR1 transcription start site following 5-aza-CdR treatment. Analogous studies using primary mouse erythroblasts derived from BFU-Es gave similar results, with 5-aza-CdR treatment leading to increased TfR1 and ferrochelatase expression, c-Myc translocation to the nucleus and increased c-Myc binding activity to TfR1 promoter. Taken together, these studies point to an important role for c-Myc in the regulation of TfR1 during erythroid differentiation induced by demethylation. Precisely how demethylation is linked to alterations in c-Myc activity is under investigating. Disclosures: No relevant conflicts of interest to declare.
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- 2010
360. Both Nramp1 and Dmt1 Are Necessary for Efficient Macrophage Iron Recycling
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Guangjun Nie, Shan Soe-Lin, Sameer S. Apte, Lidia K. Kayembe, Prem Ponka, and Marc Mikhael
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biology ,Membrane transport protein ,Endosome ,Ebselen ,digestive, oral, and skin physiology ,Immunology ,Ferroportin ,Cell Biology ,Hematology ,DMT1 ,Biochemistry ,Erythrophagocytosis ,Cell biology ,chemistry.chemical_compound ,Downregulation and upregulation ,chemistry ,parasitic diseases ,biology.protein ,Macrophage - Abstract
Abstract 1994 Poster Board I-1016 Divalent metal transporter 1 (DMT1) and natural resistance-associated macrophage protein 1 (Nramp1) are iron transporters that localize, respectively, to the early and late endosomal compartments. DMT1 is ubiquitously expressed, while Nramp1 is found only within macrophages and neutrophils. Our previous studies have identified a role for Nramp1 during macrophage erythrophagocytosis; however, little is known about the function of DMT1 during this process. Wild-type RAW264.7 macrophages (Nramp1-/-), and those stably transfected with Nramp1 (Nramp1+/+) were treated with either DMT1-siRNA, or with ebselen, a selective inhibitor of DMT1. While macrophages lacking either functional DMT1 or Nramp1 experienced a moderate reduction in iron recycling efficiency, the ability of macrophages lacking both functional DMT1 and Nramp1 to recycle hemoglobin-derived iron was severely compromised. Compared to macrophages singly deficient in either DMT1 or Nramp1 transport ability, macrophages where DMT1 and Nramp1 were both compromised exhibited an abrogated increase in labile iron pool content, released less iron, and experienced diminished upregulation of ferroportin and heme-oxygenase 1 levels following erythrophagocytosis. These results suggest that while the loss of either Nramp1 or DMT1 transport ability results in minor impairment following erythrophagocytosis, the simultaneous loss of both Nramp1 and DMT1 iron transport activity is detrimental to the iron recycling capacity of the macrophage. Disclosures: No relevant conflicts of interest to declare.
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- 2009
361. Effects of Mitochondrial Ferritin Expression on Tumor Iron Metabolism and Tumor Growth in Nude Mice Xenografts
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Guangjun Nie, Kostas Pantopoulos, Alex D. Sheftel, Guohua Chen, and Prem Ponka
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biology ,Immunology ,MITOCHONDRIAL FERRITIN ,Transferrin receptor ,Cell Biology ,Hematology ,Mitochondrion ,Biochemistry ,Cell biology ,Ferritin ,Cytosol ,chemistry.chemical_compound ,chemistry ,Frataxin ,biology.protein ,Heme ,Intracellular - Abstract
Mitochondrial ferritin (MtFt) is a mitochondrial iron storage protein, whose function and regulation is largely unknown. Our previous results have shown that MtFt markedly affects intracellular iron distribution and homeostasis in mammalian cells (Blood105: 2161–2167, 2005). Using tumor xenografts, we examined the effects of expression MtFt on tumor iron metabolism and growth. H1299 parental or MtFt overexpressing cells were implanted into nude mice. As compared to control tumor xenografts, the expression of MtFt dramatically reduced the implanted tumor growth. A cytosolic iron starvation phenotype in MtFt expressing tumors was revealed by increased RNA-binding activity of iron regulatory proteins (IRPs) and, concomitantly, both an increase in transferrin receptor levels and a decrease in cytosolic ferritin. MtFt overexpression also led to a decrease in both total cellular heme content and heme oxygenase-1 levels. In addition, the expression of MtFt in tumors was associated with a decrease in aconitase activity and lower frataxin protein levels. Mitochondrial iron deposition in MtFt expressing tumors was directly observed by transmission electron microscopy. The pattern of iron accumulation in MtFt overexpressing tumor cells is remarkably similar to that observed in the mitochondria of sideroblastic anemia patients. In conclusion, our study shows that MtFt expression significantly affected tumor iron homeostasis by shunting iron into mitochondria; iron scarcity resulted in partial defects in heme and iron-sulfur cluster syntheses. It is likely that deprivation of iron in the cytosol is the cause of the significant inhibition of xenograft tumor growth.
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- 2005
362. DMT1 Mutation in a Patient with Hypochromic Microcytic Anemia: Functional Consequences and Response to Erythropoietin
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Dagmar Pospisilova, Josef T. Prchal, Guangjun Nie, Vladimir Divoky, Prem Ponka, Martha P. Mims, Monika Priwitzerova, and Alex D. Sheftel
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Mutation ,biology ,Point mutation ,Chinese hamster ovary cell ,digestive, oral, and skin physiology ,Immunology ,Cell Biology ,Hematology ,DMT1 ,medicine.disease_cause ,Biochemistry ,Molecular biology ,Hypochromic microcytic anemia ,Exon ,Erythropoietin ,biology.protein ,medicine ,Hemoglobin ,medicine.drug - Abstract
We have previously described a case of severe hypochromic microcytic anemia caused by a homozygous mutation in the divalent metal transporter 1 ( DMT1 1285G>C ). This mutation encodes for an amino acid substitution (E399D) and causes preferential skipping of exon 12 during processing of the DMT1 mRNA. To examine the functional consequences of this mutation, full length DMT1 transcript with the patient’s point mutation or a DMT1 transcript with exon 12 deleted was expressed in Chinese hamster ovary (CHO) cells. Our results demonstrate that the E399D substitution has no effect on protein expression and function. In contrast, deletion of exon 12 led to a decreased expression of the protein and disruption of its subcellular localization and iron uptake activity. We hypothesize that the residual protein in hematopoietic cells represents the functional E399D DMT1 variant, but because of its quantitative reduction, the iron uptake activity of DMT1 in the patient’s erythroid cells is severely suppressed. Because of the positive effect of erythropoietin (EPO) on the growth of patient’s BFU-Es in our in vitro studies, we have treated the patient with recombinant human EPO. The dose of 1.2 μg/kg given once a week did not lead to any improvement in hemoglobin level. However, doubling the dose of EPO (2.4 μg/kg) led to an increase in hemoglobin level from 75 to 91 g/L and to an improvement in the patient’s clinical condition.
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- 2005
363. Overexpression of Mitochondrial Ferritin Causes Cytosolic Iron Starvation and Changes Cellular Iron Homeostatis
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Guangjun Nie, Alex D. Sheftel, Sangwon F. Kim, and Prem Ponka
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Immunology ,Cell Biology ,Hematology ,Biochemistry - Abstract
Cytosolic ferritin is well known to sequester and store iron and, consequently, protect cells against iron-mediated free radical damage. However, the function of the newly discovered mitochondrial ferritin (MtFt) is unknown. To examine the role of MtFt in cellular iron metabolism, we established a cell line that stably overexpresses the mouse MtFt under the control of tetracycline. The overexpression of MtFt caused a dose-dependent iron deficiency in the cytosol that was revealed by increased RNA-biding activity of iron regulatory proteins (IRPs) with a concomitant increase in transferrin receptor levels and a decrease in cytosolic ferritin. Consequently, the induction of MtFt resulted in a dramatic increase (2-fold) in cellular iron uptake from transferrin, most of which ended up in MtFt within mitochondria. Similarly, the induction of MtFt caused a shift of iron from cytosolic ferritin to MtFt. Moreover, the cell permeable iron chelator salicylaldehyde isonicotinoyl hydrazone (SIH) mobilized approximately twice as much iron from wild-type cells as compared to those overexpressing MtFt suggesting that iron in this protein is less accessible to SIH. Furthermore, the expression of MtFt was associated with a decrease in the activity of both mitochondrial and cytosolic aconitase activity, the latter being in agreement with the increase of IRP binding activity. In conclusion, our results indicate that the overexpression of MtFt causes a dramatic change in intracellular iron homeostasis and that the shunt of iron to mitochondrial storage protein likely limits its availability for functional iron proteins.
- Published
- 2004
364. Nanopore film based enrichment and quantification of low abundance hepcidin from human bodily fluids.
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Jia Fan, Shiwen Niu, Ailian Dong, Jian Shi, Hung-Jen Wu, Fine, Daniel H., Yaping Tian, Chunxi Zhou, Xuewu Liu, Tong Sun, Anderson, Gregory J., Ferrari, Mauro, Guangjun Nie, Ye Hu, and Yuliang Zhao
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NANOPORES ,HEPCIDIN ,PEPTIDE hormones ,BIOMARKERS ,ELECTROSTATIC interaction ,INFLAMMATION ,THERAPEUTICS - Abstract
Endogenous peptides that represent biological and pathological information of disease have attracted interest for diagnosis. However, the extraction of those low abundance peptides is still a challenge because of the complexity of human bodily fluids (HBF). Hepcidin, a peptide hormone, has been recognized as a biomarker for iron-related diseases. There is no rapid and reliable way to enrich them from HBF. Here we describe a peptide extraction approach based on nanoporous silica thin films to successfully detect hepcidin from HBF. Cooperative functions of nanopore to biomolecule, including capillary adsorption, size-exclusion and electrostatic interaction, were systematically investigated to immobilize the target peptide. To promote this new approach to clinical practices, we further applied it to successfully assay the hepcidin levels in HBF provided by healthy volunteers and patients suffering from inflammation. Our finding provides a high-throughput, rapid, label-free and cost-effective detection method for capturing and quantifying low abundance peptides from HBF. [ABSTRACT FROM AUTHOR]
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- 2014
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365. Distinct Effects of Tea Catechins on 6-Hydroxydopamine-Induced Apoptosis in PC12 Cells
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Baolu Zhao, Chao-Fang Jin, Guangjun Nie, Sheng-Rong Shen, and Yuanlin Cao
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Programmed cell death ,Antioxidant ,Cell Survival ,Polymers ,medicine.medical_treatment ,Cell ,Biophysics ,Tetrazolium Salts ,Apoptosis ,DNA Fragmentation ,Pharmacology ,Biology ,medicine.disease_cause ,Neuroprotection ,PC12 Cells ,Biochemistry ,Catechin ,Beverages ,Adrenergic Agents ,Phenols ,medicine ,Animals ,Viability assay ,Coloring Agents ,Oxidopamine ,Molecular Biology ,Cell Nucleus ,Electrophoresis, Agar Gel ,Flavonoids ,Hydroxydopamine ,Dose-Response Relationship, Drug ,food and beverages ,Flow Cytometry ,Rats ,Thiazoles ,medicine.anatomical_structure ,Models, Chemical ,Oxidative stress - Abstract
Green tea polyphenols have aroused considerable attention in recent years for preventing oxidative stress related diseases including cancer, cardiovascular disease, and degenerative disease. Neurodegenerative diseases are cellular redox status dysfunction related diseases. The present study investigated the different effects of the five main components of green tea polyphenols on 6-hydroxydopamine (6-OHDA)-induced apoptosis in PC12 cells, the in vitro model of Parkinson's disease (PD). When the cells were treated with five catechins respectively for 30 min before exposure to 6-OHDA, (-)-epigallocatechins gallate (EGCG) and (-)-epicatechin gallate (ECG) in 50-200 microM had obvious concentration-dependent protective effects on cell viability, while (-)-epicatechin (EC), (+)-catechin ((+)-C), and (-)-epigallocatechin (EGC) had almost no protective effects. The five catechins also showed the same pattern described above of the different effects against 6-OHDA-induced cell apoptotic characteristics as analyzed by cell viability, fluorescence microscopy, flow cytometry, and DNA fragment electrophoresis methods. The present results indicated that 200 microM EGCG or ECG led to significant inhibition against typical apoptotic characteristics of PC12 cells, while other catechins had little protective effect against 6-OHDA-induced cell death. Therefore, the classified protective effects of the five catechins were in the order ECGor = EGCGECor = (+)-CEGC. The antiapoptotic activities appear to be structurally related to the 3-gallate group of green tea polyphenols. The present data indicate that EGCG and ECG might be potent neuroprotective agents for PD.
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- 2002
366. How can nanotechnology help membrane vesicle-based cancer immunotherapy development?
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Xin Tian, Motao Zhu, and Guangjun Nie
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- 2013
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367. Controlling Assembly of Paired Gold Clusters within Apoferritin Nanoreactor for in Vivo Kidney Targeting and Biomedical Imaging.
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Cuiji Sun, Hui Yang, Hui Yuan, Xin Tian, Liming Wang, Yi Guo, Li Xu, Jian Lei, Ning Gao, Anderson, Gregory J., Xing-Jie Liang, Chunying Chen, Yuliang Zhao, and Guangjun Nie
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- 2011
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368. Lysosomal Proteolysis Is the Primary Degradation Pathway for Cytosolic Ferritin and Cytosolic Ferritin Degradation Is Necessary for Iron Exit.
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Yinghui Zhang, Marc Mikhael, Dongxue Xu, Yiye Li, Shan Soe-Lin, Bo Ning, Wei Li, Guangjun Nie, Yuliang Zhao, and Prem Ponka
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- 2010
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369. Neuroprotective Mechanism of Mitochondrial Ferritin on 6-Hydroxydopamine–Induced Dopaminergic Cell Damage: Implication for Neuroprotection in Parkinson's Disease.
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Zhen-Hua Shi, Guangjun Nie, Xiang-Lin Duan, Tracey Rouault, Wen-Shuang Wu, Bo Ning, Nan Zhang, Yan-Zhong Chang, and Bao-Lu Zhao
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FERRITIN , *CELL death , *NERVOUS system , *PURKINJE cells , *GENOTYPE-environment interaction , *PEROXIDATION , *OXIDATIVE stress - Abstract
AbstractNeuronal iron homeostasis disruption and oxidative stress are closely related to the pathogenesis of Parkinson's disease (PD). Adult iron-regulatory protein 2 knockout (Ireb2–/–) mice develop iron accumulation in white matter tracts and nuclei in different brain area and display severe neurodegeneration in Purkinje cells of the cerebrum. Mitochondrial ferritin (MtFt), a newly discovered ferritin, specifically expresses in high energy–consuming cells, including neurons of brain and spinal cord. Interestingly, the decreased expression of MtFt in cerebrum, but not in striatum, matches the differential neurodegeneration pattern in these Ireb2–/–mice. To explore its effect on neurodegeneration, the effects of MtFt expression on 6-hydrodopamine (6-OHDA)-induced neuronal damage was examined. The overexpression of MtFt led to a cytosolic iron deficiency in the neuronal cells and significantly prevented the alteration of iron redistribution induced by 6-OHDA. Importantly, MtFt strongly inhibited mitochondrial damage, decreased production of the reactive oxygen species and lipid peroxidation, and dramatically rescued apoptosis by regulating Bcl-2, Bax and caspase-3 pathways. In conclusion, this study demonstrates that MtFt plays an important role in preventing neuronal damage in an 6-OHDA–induced parkinsonian phenotype by maintaining iron homeostasis. Regulation of MtFt expression in neuronal cells may provide a new neuroprotective strategy for PD. Antioxid. Redox Signal.13, 783–796. [ABSTRACT FROM AUTHOR]
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- 2010
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370. Overexpression of Mitochondrial Ferritin Sensitizes Cells to Oxidative Stress Via an Iron-Mediated Mechanism.
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Zhongbing Lu, Guangjun Nie, Yiye Li, Shan Soe–lin, Yi Tao, Yuanlin Cao, Zhiyong Zhang, Nianqing Liu, Prem Ponka, and Baolu Zhao
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FERRITIN , *GENE expression , *MITOCHONDRIA , *OXIDATIVE stress , *IRON in the body , *HOMEOSTASIS , *BIOTRANSFORMATION (Metabolism) - Abstract
AbstractMitochondrial ferritin (MtFt) is a newly identified H-ferritin-like protein expressed only in mitochondria. Previous studies have shown that its overexpression markedly affects intracellular iron homeostasis and rescues defects caused by frataxin deficiency. To assess how MtFt exerts its function under oxidative stress conditions, MtFt overexpressing cells were treated with tert-butyl-hydroperoxide (tBHP), and the effects of MtFt expression on cell survival and iron homeostasis were examined. We found that MtFt expression was associated with decreased mitochondrial metabolic activity and reduced glutathione levels as well as a concomitant increase in reactive oxygen species levels and apoptosis. Moreover, mechanistic studies demonstrated that tBHP treatment led to a prolonged decrease in cytosolic ferritins levels in MtFt-expressing cells, while ferritin levels recovered to basal levels in control counterparts. tBHP treatment also resulted in elevated transferrin receptors, followed by more iron acquisition in MtFt expressing cells. The high molecular weight desferrioxamine, targeting to lysosomes, as well as the hydrophobic iron chelator salicylaldehyde isonicotinoyl hydrazone significantly attenuated tBHP-induced cell damage. In conclusion, the current study indicates that both the newly acquired iron from the extracellular environment and internal iron redistribution from ferritin degradation may be responsible for the increased sensitivity to oxidative stress in MtFt-expressing cells. Antioxid. Redox Signal.11, 1791–1803. [ABSTRACT FROM AUTHOR]
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- 2009
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371. Targeted degradation of LRG1 to attenuate renal fibrosis.
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Linyao Fan, Yingqiu Qi, Xi Yang, Yarui Xu, Yana Zhang, Longdi Wang, Anying Zhu, Lirong Zhang, Jian Song, Shengnan Du, Guangjun Nie, and Huan Min
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RENAL fibrosis , *PEPTIDES , *CELLULAR signal transduction , *LENALIDOMIDE , *PROTEOLYSIS - Abstract
Leucine-rich α-2 glycoprotein 1 (LRG1), a secreted glycoprotein, has been identified as significantly upregulated in renal fibrosis, potentially exacerbating the condition by enhancing TGF-β-Smad3-dependent signaling pathways. Herein, utilizing our developed LRG1-targeting peptide for LRG1 recruitment and lenalidomide for E3 ubiquitin ligase engagement, we developed an advanced proteolysis targeting chimera, ET TAC-2, specifically designed for LRG1 degradation. Our cellular degradation assays validated that ET TAC-2 effectively degraded LRG1 through a proteasome-dependent mechanism, achieving halfmaximal degradation at a concentration of 8.38 μM. Furthermore, anti-fibrotic experiments conducted both in vitro and in vivo revealed that ET TAC-2 efficiently induced LRG1 degradation in fibrotic kidneys. This action effectively inhibited the TGF-β-Smad3 signaling pathway and diminished the secretion of fibrosis-associated proteins, consequently attenuating the progression of renal fibrosis. Our study highlights the pivotal role of LRG1 in renal fibrosis and positions ET TAC-2 as a promising therapeutic candidate for targeted LRG1 intervention. [ABSTRACT FROM AUTHOR]
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- 2024
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372. Antineoplastic activities of Gd@C82(OH)22 nanoparticles: tumor microenvironment regulation
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Guangjun Nie, Yiye Li, and YanHuan H. Tian
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Tumor microenvironment ,Biocompatibility ,Agricultural and Biological Sciences(all) ,Chemistry ,Biochemistry, Genetics and Molecular Biology(all) ,Rational design ,Nanoparticle ,General Biochemistry, Genetics and Molecular Biology ,Environmental Science(all) ,Immunology ,Cancer cell ,Cancer research ,Nanomedicine ,Tumor cytotoxicity ,Tumor growth ,General Agricultural and Biological Sciences ,General Environmental Science - Abstract
Malignant tumors are complex organs consisting of tumor cells and their microenvironment. Increasing evidence has shown that the tumor microenvironment is critical to the initiation and progression of tumors. Rational design of tumor therapies via targeting the tumor microenvironment to inhibit tumor growth is thus becoming a consensus strategy. Gd@C(82)(OH)(22) nanoparticles, as novel endohedral hydroxylated metallofullerenes, have been demonstrated to be a potent antitumor nanomedicine via targeting multiple factors in the tumor microenvironment. Gd@C(82)(OH)(22) nanoparticles possess excellent biocompatibility and remarkable antineoplastic activity, as a result not of direct tumor cytotoxicity but of their diverse biological effects, including antioxidation, immune activation, angiogenesis inhibition, imprisoning cancer cells, and reversal of drug-resistance. In this article, we summarize the unique nanoscale physiochemical properties and the antineoplastic activities of Gd@C(82)(OH)(22) nanoparticles, and focus on the mechanisms underlying their regulation of the tumor microenvironment.
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373. Biomaterial design for regenerating aged bone: materiobiological advances and paradigmatic shifts.
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(戴凯), Kai Dai, (耿振), Zhen Geng, (张文超), Wenchao Zhang, (魏雪), Xue Wei, (王靖), Jing Wang, (聂广军), Guangjun Nie, and (刘昌胜), Changsheng Liu
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BIOMATERIALS , *BONE regeneration , *REGENERATION (Biology) , *BONE diseases , *POPULATION aging , *BLOOD vessels , *QUALITY of life - Abstract
China's aging demographic poses a challenge for treating prevalent bone diseases impacting life quality. As bone regeneration capacity diminishes with age due to cellular dysfunction and inflammation, advanced biomaterials-based approaches offer hope for aged bone regeneration. This review synthesizes materiobiology principles, focusing on biomaterials that target specific biological functions to restore tissue integrity. It covers strategies for stem cell manipulation, regulation of the inflammatory microenvironment, blood vessel regeneration, intervention in bone anabolism and catabolism, and nerve regulation. The review also explores molecular and cellular mechanisms underlying aged bone regeneration and proposes a database-driven design process for future biomaterial development. These insights may also guide therapies for other age-related conditions, contributing to the pursuit of 'healthy aging'. [ABSTRACT FROM AUTHOR]
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- 2024
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374. Recent Advances of Nanocarriers for Effective Delivery of Therapeutic Peptides
- Author
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Mona Atabakhshi-Kashi, Mohammad Taleb, Guangjun Nie, Yinlong Zhang, Yazhou Wang, Hamidreza Akhbariyoon, Khosro Khajeh, and Marzieh Geranpayehvaghei
- Subjects
lcsh:Medical technology ,lcsh:R855-855.5 ,Computer science ,lcsh:R ,General Engineering ,lcsh:Medicine ,Computational biology ,Nanocarriers ,Small molecule - Abstract
Precisely selective interactions of peptides with their unique binding partners represent an out-standing starting point for designing novel therapeutics. It is well established that peptides with a variety of critical physiological functions and specific mechanisms of action offer distinct ad-vantages, including excellent safety and higher efficiency over traditional small molecule thera-peutics. Certain intrinsic weaknesses of naturally occurring peptides such as negligible plasma half-life, low bioavailability, and potential immunogenicity have limited their administration as medicines. Nanotechnology has expanded several promising strategies to address the limitations associated with therapeutic peptides. This review aims to perform a state-of-the-art summary of the strategies that are actively used to develop efficient formulations of nanosystem based pep-tide medicines. We first focus on the recent advances and updates on peptide-based nanomedi-cines. Then we indicate how nanosystems improved the functionality of therapeutic peptides and what the future opportunities and challenges of developments in the field of therapeutic pep-tides are. Potential noninvasive delivery platforms for peptide incorporated nanoparticles through alternative administration routes are also discussed.
375. 5-Aza-2'-deoxycytidine Activates Iron Uptake and Heme Biosynthesis by Increasing c-Myc Nuclear Localization and Binding to the E-boxes of Transferrin Receptor 1 (TfR1) and Ferrochelatase (Fech) Genes.
- Author
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Bo Ning, Gang Liu, Yuanyuan Liu, Xiufen Su?, Anderson, Gregory J., Xin Zheng, Yanzhong Chang, Mingzhou Guo, Yuanfang Liu, Yuliang Zhao, and Guangjun Nie
- Subjects
- *
HEME , *BIOSYNTHESIS , *MYELODYSPLASTIC syndromes , *ANEMIA , *ERYTHROCYTE membranes , *TRANSCRIPTION factors - Abstract
The hypomethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) and its derivatives have been successfully used for the treatment of myelodysplastic syndromes, and they frequently improve the anemia that usually accompanies these disorders. However, the molecular mechanisms underlying this action remain poorly understood. In this study, we used two erythroid models, murine erythroid leukemia cells and erythroid burst-forming unit-derived erythroblasts, to show that 5-aza-CdR induced erythroid differentiation and increased the expression of transferrin receptor 1 (TfR1) and ferrochelatase (Fech), thereby increasing iron uptake and heme biosynthesis. We have identified new regulatory E-boxes that lie outside of CpG islands in the TfR1 and Fech promoters, and the methylation status of these sites can be altered by 5-aza-CdR treatment. This in turn altered the binding of the transcription factor c-Myc to these promoter elements. Furthermore, 5-aza-CdR promoted the nuclear translocation of c-Myc and its binding to Max to form functional complexes. The coordinated actions of 5-aza-CdR on the methylation status of the target genes and in stimulating the nuclear translocation of c-Myc provide new molecular insights into the regulation of E-boxes and explain, at least in part, the increased erythroid response to 5-aza-CdR treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2011
- Full Text
- View/download PDF
376. Ferroportini deficiency in mouse macrophages impairs iron homeostasis and inflammatory responses.
- Author
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Zhuzhen Zhang, Fan Zhang, Peng An, Xin Guo, Yuanyuan Shen, Yunlong Tao, Qian Wu, Yuchao Zhang, Yu Yu, Bo Ning, Guangjun Nie, Knutson, Mitchell D., Anderson, Gregory J., and Fudi Wang
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LABORATORY mice , *MACROPHAGES , *HOMEOSTASIS , *PHENYLHYDRAZINE , *IRON deficiency diseases - Abstract
Systemic iron requirements are met predominantly through the recycling of iron from senescent erythrocytes by macrophages, a process in which the iron exporter ferroportin (Fpn1) is considered to be essential. Yet the role of Fpn1 in macrophage iron recycling and whether it influences innate immune responses are poorly understood in vivo. We inactivated Fpn1 in macrophages by crossing Fpn1-floxed animals with macrophage-targeted LysM-Cre or F4/80-Cre transgenic mice. Macrophage Fpn1 deletion mice were overtly normal; however, they displayed a mild anemia and iron accumulation in splenic, hepatic, and bone marrow macrophages when fed a standard diet. Iron loading was exacerbated after the administration of iron dextran or phenylhydrazine. When Fpn1LysM/LysM mice were challenged with an iron-deficient diet, they developed a more severe anemia and strikingly higher splenic iron levels than control mice, indicating significantly impaired iron mobilization from macrophages. Because immune responses can be altered by modulating iron status, we also examined the expression of proinflammatory cytokines. We found that expression levels of TNF-α and IL-6 were significantly enhanced in Fpn1LysM/LysM macrophages lacking Fpn1. These studies demonstrate that Fpn1 plays important roles in macrophage iron release in vivo and in modulating innate immune responses. [ABSTRACT FROM AUTHOR]
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- 2011
- Full Text
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377. Heterozygous missense mutations in the GLRX5 gene cause sideroblastic anemia in a Chinese patient.
- Author
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Gang Liu, Shanshan Guo, Anderson, Gregory J., Camaschella, Clara, Bing Han, and Guangjun Nie
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ANEMIA , *MISSENSE mutation , *GENETIC carriers , *PATIENTS - Abstract
A letter to the editor is presented which discusses the case of a Chinese patient with congenital sideroblastic anemia (CSA) caused by heterozygote missense mutations in his GLRX5 gene.
- Published
- 2014
- Full Text
- View/download PDF
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