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Jung‐Il Chae Janghwan Kim Sun‐Mi Woo Hyo‐Won Han Young Keun Cho Keon‐Bong Oh Ki‐Hoan Nam Yong‐Kook Kang 《Proteomics》2009,9(5):1128-1141
The ability to generate neural lineages from human embryonic stem cells (hESCs) in a controlled manner would further investigation of human neurogenesis and development of potential cell therapeutic applications to treat neurological diseases; however, generating such neural stem cells (NSCs) remains a challenge. In an attempt to characterize the cellular mechanisms involved in hESC differentiation into neuroprogenitor cells, we performed 2‐DE using protein extracts from hESC‐derived embryoid bodies (EBs) and neuroectodermal spheres (NESs) bearing neuroprogenitors. Of 47 differentially expressed protein spots, 28 nonredundant spots were shown to be upregulated in the NESs; these protein spots included neurogenesis‐related proteins (TAF1, SEPT2, NPH3, and CRABP), as expected. Interestingly, 6 of these 28 protein spots were cytoskeleton‐associated proteins (CSAP) such as Fascin‐1, Cofilin‐1, and Stathmin‐1. Western‐blot analyses confirmed the increased levels of these proteins in the NESs. Furthermore, immunostaining analysis showed that both Fascin‐1 and Stathmin‐1 were preferentially expressed in the inner rims of neural rosettes, which are characteristic features of neuroprogenitors in culture. We also confirmed prominent expression of Fascin‐1 in (sub‐)ventricular zone in E15.5 mouse fetal brain. Our results suggest that, in addition to the induction of those genes involved in neural development, hESC differentiation into the NES is associated with a marked reorganization of the cellular cytoskeleton. 相似文献
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Songlin Zeng Huan Zhang Zhen Ding Rui Luo Kang An Lianzeng Liu Jing Bi Huanchun Chen Shaobo Xiao Liurong Fang 《Proteomics》2015,15(11):1819-1828
Porcine epidemic diarrhea virus (PEDV) causes an acute, highly contagious, and devastating viral enteric disease with a high mortality rate in suckling pigs. A large‐scale outbreak of PED occurred in China in 2010, with PEDV emerging in the United States in 2013 and spreading rapidly, posing significant economic and public health concerns. In this study, LC–MS/MS coupled to iTRAQ labeling was used to quantitatively identify differentially expressed cellular proteins in PEDV‐infected Vero cells. We identified 49 differentially expressed cellular proteins, of which 8 were upregulated and 41 downregulated. These differentially expressed proteins were involved in apoptosis, signal transduction, and stress responses. Based on these differentially expressed proteins, we propose that PEDV might utilize apoptosis and extracellular signal regulated kinases pathways for maximum viral replication. Our study is the first attempt to analyze the protein profile of PEDV‐infected cells by quantitative proteomics, and we believe our findings provide valuable information with respect to better understanding the host response to PEDV infection. 相似文献
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Jinghui Jia Jingyu Wang Ming Teh Wei Sun Jianhua Zhang Irene Kee Pierce K.‐H. Chow Rosa Cynthia M.‐Y. Liang Maxey C. M. Chung Ruowen Ge 《Proteomics》2010,10(2):224-234
Hepatocellular carcinoma (HCC) is one of the deadliest cancers with few treatment options. It is a hypervascular tumor in which angiogenesis plays a critical role in its progression. Tumor capillary endothelial cells (TECs) in HCC are known to originate from liver sinusoid endothelial cells, which then go through a capillarization process to become morphologically as well as functionally different TECs. In this work, we investigated proteins differentially expressed between freshly isolated TECs and sinusoid endothelial cells from well‐formed rat HCC using 2‐D DIGE coupled with MALDI‐TOF/TOF MS. Thirty‐eight unique proteins were identified to be differentially expressed more than twofold between the two endothelial cell types. Amongst the differentially expressed proteins, two novel endothelial markers, EH domain‐containing protein 3 and galectin‐3, were confirmed by Western blot and immunohistochemistry in both rat and human HCC samples. We showed that EH domain‐containing protein 3 is significantly down‐regulated in TECs, but galectin‐3 is up‐regulated. We propose possible roles of these two proteins in tumor vessel development in HCC. 相似文献
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Joao A. Paulo Raul Urrutia Vivek Kadiyala Peter Banks Darwin L. Conwell Hanno Steen 《Proteomics》2013,13(9):1499-1512
Toxic compounds in tobacco, such as nicotine, may adversely affect pancreatic function. We aim to determine nicotine‐induced protein alterations in pancreatic cells, thereby revealing links between nicotine exposure and pancreatic disease. We compared the proteomic alterations induced by nicotine treatment in cultured pancreatic cells (mouse, rat, and human stellate cells and human duct cells) using MS‐based techniques, specifically SDS‐PAGE (gel) coupled with LC‐MS/MS and spectral counting. We identified thousands of proteins in pancreatic cells, hundreds of which were identified exclusively or in higher abundance in either nicotine‐treated or untreated cells. Interspecies comparisons of stellate cell proteins revealed several differentially abundant proteins (in nicotine treated versus untreated cells) common among the three species. Proteins appearing in all nicotine‐treated stellate cells include amyloid beta (A4), procollagen type VI alpha 1, integral membrane protein 2B, and toll‐interacting protein. Proteins that were differentially expressed upon nicotine treatment across cell lines were enriched in certain pathways, including nicotinic acetylcholine receptor, cytokine, and integrin signaling. At this analytical depth, we conclude that similar pathways are affected by nicotine, but alterations at the protein level among stellate cells of different species vary. Further interrogation of such pathways will lead to insights into the potential effect of nicotine on pancreatic cells at the biomolecular level and the extension of this concept to the effect of nicotine on pancreatic disease. 相似文献
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Marica Gemei Claudia Corbo Francesca D'Alessio Rosa Di Noto Renza Vento Luigi Del Vecchio 《Proteomics》2013,13(22):3293-3297
Cancer stem cell characterization represents a breakthrough in cancer research. Despite evidence showing the existence and the role of cancer stem cells in osteosarcoma (OS) onset and progression, little is known about their specific surface phenotype. To address this issue, we carried out a cytometric analysis with an antibody‐array comprising 245 membrane proteins comparing the stem and differentiated OS cells. As experimental model, we chose the stem‐like cell line 3aminobenzamide‐OS and its parental, differentiated, cell line MG63. We identified 50 differentially expressed, 23 homogeneously expressed, and 172 not expressed proteins in the two cell line models, thus defining a surface protein signature specific for each of them. Furthermore, we selected ERK1/2 (p44/42 mitogen‐activated protein kinases) as a potential pathway correlated with processes that characterize tumorigenic potential and stemness of 3aminobenzamide‐OS cells. 相似文献
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Cell penetrating peptides (CPP) have been widely used to increase the cellular delivery of their associated cargo. Multiple modes of uptake have been identified; however, they cannot be predicted a priori. Elucidating these mechanisms is important for understanding peptide function as well as further optimizing cellular delivery. We have developed a class of mitogen activated protein kinase activated protein kinase 2 (MK2) inhibitor peptides, named FAK and YARA that utilize CPP domains to gain cellular access. In this study, we investigate the mechanism of endocytosis of these MK2 inhibitors by examining the uptake of fluorescently labeled peptide in human monocyte (THP‐1) and mesothelial cells, and looking for colocalization with known markers of endocytosis. Our results indicate that uptake of the MK2 inhibitors was minimally enhanced by the addition of the fluorescent label, and that the type of endocytosis used by the inhibitor depends on several factors including concentration, cell type, and which CPP was used. We found that in THP‐1 cells, the uptake of YARA occurred primarily via macropinocytosis, whereas FAK entered via all three mechanisms of endocytosis examined in this study. In mesothelial cells, uptake of YARA occurred via caveolae‐mediated endocytosis, but became less specific at higher concentrations; whereas uptake of FAK occurred through clathrin‐mediated endocytosis. In all cases, the delivery resulted in active inhibition of MK2. In summary, the results support endocytic uptake of fluorescently labeled FAK and YARA in two different cell lines, with the mechanism of uptake dependent on extracellular concentration, cell type, and choice of CPP. Copyright © 2013 European Peptide Society and John Wiley & Sons, Ltd. 相似文献
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Mitochondrial proteomics with siRNA knockdown to reveal ACAT1 and MDH2 in the development of doxorubicin‐resistant uterine cancer
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Shing‐Jyh Chang Chia‐Hao Chan Kevin W. Lyu Jo‐Fan Chang Eugenie Wong Soon May Dai‐Ying Lin Hsiu‐Chuan Chou Hong‐Lin Chan 《Journal of cellular and molecular medicine》2015,19(4):744-759
Mitochondria are key organelles in mammary cells in responsible for a number of cellular functions including cell survival and energy metabolism. Moreover, mitochondria are one of the major targets under doxorubicin treatment. In this study, low‐abundant mitochondrial proteins were enriched for proteomic analysis with the state‐of‐the‐art two‐dimensional differential gel electrophoresis (2D‐DIGE) and matrix‐assistant laser desorption ionization time‐of‐flight mass spectrometry (MALDI‐TOF MS) strategy to compare and identify the mitochondrial protein profiling changes in response to the development of doxorubicin resistance in human uterine cancer cells. The mitochondrial proteomic results demonstrate more than fifteen hundred protein features were resolved from the equal amount pooled of three purified mitochondrial proteins and 101 differentially expressed spots were identified. In which, 39 out of these 101 identified proteins belong to mitochondrial proteins. Mitochondrial proteins such as acetyl‐CoA acetyltransferase (ACAT1) and malate dehydrogenase (MDH2) have not been reported with the roles on the formation of doxorubicin resistance in our knowledge. Further studies have used RNA interference and cell viability analysis to evidence the essential roles of ACAT1 and MDH2 on their potency in the formation of doxorubicin resistance through increased cell viability and decreased cell apoptosis during doxorubicin treatment. To sum up, our current mitochondrial proteomic approaches allowed us to identify numerous proteins, including ACAT1 and MDH2, involved in various drug‐resistance‐forming mechanisms. Our results provide potential diagnostic markers and therapeutic candidates for the treatment of doxorubicin‐resistant uterine cancer. 相似文献
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Impact of the mitogen‐activated protein kinase pathway on the subproteome of detergent‐resistant microdomains of colon carcinoma cells
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Christian V. Recktenwald Rudolf Lichtenfels Jens Wulfaenger Anja Müller Sven P. Dressler Barbara Seliger 《Proteomics》2015,15(1):77-88
Lipid rafts play a key role in the regulation of fundamentally important cellular processes, including cell proliferation, differentiation, and survival. The composition of such detergent‐resistant microdomains (DRMs) is altered under pathologic conditions, including cancer. Although DRMs have been analyzed in colorectal carcinoma little information exists about their composition upon treatment with targeted drugs. Hence, a quantitative proteomic profiling approach was performed to define alterations within the DRM fraction of colorectal carcinoma cells upon treatment with the drug U0126, an inhibitor of the mitogen‐activated protein kinase pathway. Comparative expression profilings resulted in the identification of 300 proteins, which could partially be linked to key oncogenic signaling pathways and tumor‐related cellular features, such as cell proliferation, adhesion, motility, invasion, and apoptosis resistance. Most of these proteins were downregulated upon inhibitor treatment. In addition, quantitative proteomic profilings of cholesterol‐depleted versus intact lipid rafts were performed to define, which U0126‐regulated target structures represent bona fide raft proteins. Selected differentially abundant raft proteins were validated at the mRNA and/or protein level using U0126‐ or Trametinib‐treated cells. The presented data provide insights into the molecular mechanisms associated with the response to the treatment with MEK inhibitors and might also lead to novel candidates for therapeutic interventions. 相似文献
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Marta Deganuto Laura Cesaratto Cristina Bellarosa Raffaella Calligaris Sandra Vilotti Giovanni Renzone Rossana Foti Andrea Scaloni Stefano Gustincich Franco Quadrifoglio Claudio Tiribelli Gianluca Tell 《Proteomics》2010,10(8):1645-1657
Unconjugated bilirubin (UCB) is a powerful antioxidant and a modulator of cell growth through the interaction with several signal transduction pathways. Although newborns develop a physiological jaundice, in case of severe hyperbilirubinemia UCB may become neurotoxic causing severe long‐term neuronal damages, also known as bilirubin encephalopathy. To investigate the mechanisms of UCB‐induced neuronal toxicity, we used the human neuroblastoma cell line SH‐SY5Y as an in vitro model system. We verified that UCB caused cell death, in part due to oxidative stress, which leads to DNA damage and cell growth reduction. The mechanisms of cytotoxicity and cell adaptation to UCB were studied through a proteomic approach that identified differentially expressed proteins involved in cell proliferation, intracellular trafficking, protein degradation and oxidative stress response. In particular, the results indicated that cells exposed to UCB undertake an adaptive response that involves DJ‐1, a multifunctional neuroprotective protein, crucial for cellular oxidative stress homeostasis. This study sheds light on the mechanisms of bilirubin‐induced neurotoxicity and might help to design a strategy to prevent or ameliorate the neuronal damages leading to bilirubin encephalopathy. 相似文献
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Oxidative stress is known to play important roles in engineered nanomaterial‐induced cellular toxicity. However, the proteins and signaling pathways associated with the engineered nanomaterial‐mediated oxidative stress and toxicity are largely unknown. To identify these toxicity pathways and networks that are associated with exposure to engineered nanomaterials, an integrated proteomic study was conducted using human bronchial epithelial cells, BEAS‐2B and nanoscale titanium dioxide. Utilizing 2‐DE and MS, we identified 46 proteins that were altered at protein expression levels. The protein changes detected by 2‐DE/MS were verified by functional protein assays. These identified proteins include some key proteins involved in cellular stress response, metabolism, adhesion, cytoskeletal dynamics, cell growth, cell death, and cell signaling. The differentially expressed proteins were mapped using Ingenuity Pathway Analyses? canonical pathways and Ingenuity Pathway Analyses tox lists to create protein‐interacting networks and proteomic pathways. Twenty protein canonical pathways and tox lists were generated, and these pathways were compared to signaling pathways generated from genomic analyses of BEAS‐2B cells treated with titanium dioxide. There was a significant overlap in the specific pathways and lists generated from the proteomic and the genomic data. In addition, we also analyzed the phosphorylation profiles of protein kinases in titanium dioxide‐treated BEAS‐2B cells for a better understanding of upstream signaling pathways in response to the titanium dioxide treatment and the induced oxidative stress. In summary, the present study provides the first protein‐interacting network maps and novel insights into the biological responses and potential toxicity and detoxification pathways of titanium dioxide. 相似文献
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Quantitative Analysis of the Global Proteome in Peripheral Blood Mononuclear Cells from Patients with New‐Onset Psoriasis
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Psoriasis is a common chronic autoimmune skin disease involving the activation of T cells. To explore the proteomic signature of peripheral blood mononuclear cells, a quantitative analysis of their global proteome was conducted in samples from Chinese patients with new‐onset psoriasis (n = 31) and healthy controls (n = 32) using an integrated quantitative approach with tandem mass tag labeling and LC–MS/MS. Protein annotation, unsupervised hierarchical clustering, functional classification, functional enrichment and cluster, and protein–protein interaction analyses were performed. A total of 5178 proteins were identified, of which 4404 proteins were quantified. The fold‐change cutoff was set at 1.2 (patients vs controls); 335 proteins were upregulated, and 107 proteins were downregulated. The bioinformatics analysis indicated that the differentially expressed proteins were involved in processes related to the activation of immune cells including the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) pathway, cellular energy metabolism, and proliferation. Three upregulated proteins and two phosphorylated proteins in the NF‐κB pathway were verified or identified by Western blotting. These results confirm that the NF‐κB pathway is critical to psoriasis. In addition, many differentially expressed proteins identified in this study have never before been associated with psoriasis, and further studies on these proteins are necessary. 相似文献
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Herein, we present the efficient cellular uptake of immobilized virus-like particles (VLPs) made of recombinant JC virus capsid proteins. VLPs expressed in Escherichia coli were labeled with fluorescein isothiocyanate (FITC). We compared two approaches for the cellular uptake of the FITC-VLPs. In the first approach, FITC-VLPs were immobilized on a polystyrene substrate, and then NIH3T3 cells were cultured on the same substrate. In the second approach, cells were cultured on a polystyrene substrate, and FITC-VLPs were then added to the cell culture medium. Flow cytometric analysis and confocal laser microscopic observation revealed that immobilized VLPs were incorporated into the cells with higher efficiency than were the diffusive VLPs suspended in solution. The cellular uptake of VLPs on the substrate was increased in a VLP density-dependent manner. As a control, disassembling VLPs to form VP1 pentamers abolished incorporation into the cells. Displaying sialic acid on the substrate enhanced VLP density through the specific affinities between the VLPs and sialic acid, resulting in efficient incorporation into the seeded cells. These techniques can be applied to the development of novel drug delivery systems and cell microarrays not only of nucleic acids but also of small molecules and proteins through their encapsulation in VLPs. 相似文献
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Gina Lisignoli Katia Codeluppi Katia Todoerti Cristina Manferdini Anna Piacentini Nicoletta Zini Francesco Grassi Luca Cattini Roberta Piva Vittorio Rizzoli Andrea Facchini Nicola Giuliani Antonino Neri 《Journal of cellular physiology》2009,220(2):401-409
Bone marrow stromal cells (MSCs) and osteoblasts are the two main non‐haematopoietic cellular components of human bone tissue. To identify novel osteoblast‐related molecules, we performed a gene expression profiling analysis comparing MSCs and osteoblasts isolated from the same donors. Genes differentially overexpressed in osteoblasts were mainly related to the negative control of cell proliferation, pro‐apoptotic processes, protein metabolism and bone remodelling. Notably, we also identified the collagen XV (COL15A1) gene as the most up‐regulated gene in osteoblasts compared with MSCs, previously described as being expressed in the basement membrane in other cell types. The expression of collagen type XV was confirmed at the protein level on isolated osteoblasts and we demonstrated that it significantly increases during the osteogenic differentiation of MSCs in vitro and that free ionised extracellular calcium significantly down‐modulates its expression. Moreover, light and electron microscopy showed that collagen type XV is expressed in bone tissue biopsies mainly by working osteoblasts forming new bone tissue or lining bone trabeculae. To our knowledge, these data represent the first evidence of the expression of collagen type XV in human osteoblasts, a calcium‐regulated protein which correlates to a specific functional state of these cells. J. Cell. Physiol. 220: 401–409, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
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Isobaric Tag‐Based Protein Profiling of a Nicotine‐Treated Alpha7 Nicotinic Receptor‐Null Human Haploid Cell Line
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Nicotinic acetylcholine receptors (nAChR), the primary cell surface targets of nicotine, have implications in various neurological disorders. Here we investigate the proteome‐wide effects of nicotine on human haploid cell lines (wildtype HAP1 and α7KO‐HAP1) to address differences in nicotine‐induced protein abundance profiles between these cell lines. We performed an SPS‐MS3‐based TMT10‐plex experiment arranged in a 2‐3‐2‐3 design with two replicates of the untreated samples and three of the treated samples for each cell line. We quantified 8775 proteins across all ten samples, of which several hundred differed significantly in abundance. Comparing α7KO‐HAP1 and HAP1wt cell lines to each other revealed significant protein abundance alterations; however, we also measured differences resulting from nicotine treatment in both cell lines. Among proteins with increased abundance levels due to nicotine treatment included those previously identified: APP, APLP2, and ITM2B. The magnitude of these changes was greater in HAP1wt compared to the α7KO‐HAP1 cell line, implying a potential role for the α7 nAChR in HAP1 cells. Moreover, the data revealed that membrane proteins and proteins commonly associated with neurons were predominant among those with altered abundance. This study, which is the first TMT‐based proteome profiling of HAP1 cells, defines further the effects of nicotine on non‐neuronal cellular proteomes. 相似文献
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Mark F. Santos Germana Rappa Jana Karbanov Cheryl Vanier Chikao Morimoto Denis Corbeil Aurelio Lorico 《Journal of cellular and molecular medicine》2019,23(6):4408-4421
The intercellular communication mediated by extracellular vesicles (EVs) has gained international interest during the last decade. Interfering with the mechanisms regulating this cellular process might find application particularly in oncology where cancer cell‐derived EVs play a role in tumour microenvironment transformation. Although several mechanisms were ascribed to explain the internalization of EVs, little is our knowledge about the fate of their cargos, which are crucial to mediate their function. We recently demonstrated a new intracellular pathway in which a fraction of endocytosed EV‐associated proteins is transported into the nucleoplasm of the host cell via a subpopulation of late endosomes penetrating into the nucleoplasmic reticulum. Silencing tetraspanin CD9 both in EVs and recipient cells strongly decreased the endocytosis of EVs and abolished the nuclear transfer of their cargos. Here, we investigated whether monovalent Fab fragments derived from 5H9 anti‐CD9 monoclonal antibody (referred hereafter as CD9 Fab) interfered with these cellular processes. To monitor the intracellular transport of proteins, we used fluorescent EVs containing CD9‐green fluorescent protein fusion protein and various melanoma cell lines and bone marrow‐derived mesenchymal stromal cells as recipient cells. Interestingly, CD9 Fab considerably reduced EV uptake and the nuclear transfer of their proteins in all examined cells. In contrast, the divalent CD9 antibody stimulated both events. By impeding intercellular communication in the tumour microenvironment, CD9 Fab‐mediated inhibition of EV uptake, combined with direct targeting of cancerous cells could lead to the development of novel anti‐melanoma therapeutic strategies. 相似文献
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Spermatogenesis‐associated proteins at different developmental stages of buffalo testicular seminiferous tubules identified by comparative proteomic analysis
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Yu‐Lin Huang Qiang Fu Hong Pan Fu‐Mei Chen Xiu‐Ling Zhao Huan‐Jing Wang Peng‐Fei Zhang Feng‐Ling Huang Yang‐Qing Lu Ming Zhang 《Proteomics》2016,16(14):2005-2018
The testicular seminiferous tubules contain Sertoli cells and different types of spermatogenic cells. They provide the microenvironment for spermatogenesis, but the precise molecular mechanism of spermatogenesis is still not well known. Here, we have employed tandem mass tag coupled to LC‐MS/MS with the high‐throughput quantitative proteomics technology to explore the protein expression from buffalo testicular seminiferous tubules at three different developmental stages (prepuberty, puberty, and postpuberty). The results show 304 differentially expressed proteins with a ≥2‐fold change, and bioinformatics analysis indicates that 27 of these may be associated with spermatogenesis. Expression patterns of seven selected proteins were verified via Western blot and quantitative RT‐PCR analysis, and further cellular localizations of these proteins by immunohistochemical or immunofluorescence analysis. Taken together, the results provide potential molecular markers of spermatogenesis and provide a rich resource for further studies on male reproduction regulation. 相似文献
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Weijia Wang Xiuming Zhang Kaiying Deng Shifeng Huang Xiaoqin Mao Yurong Fu Zhengjun Yi Yurong Yan Zongyin Qiu 《Cell biochemistry and function》2009,27(6):329-337
A novel sterol mesylate compound (NSC67657) was recently identified and reported by National Cancer Institute that could efficiently induce the differentiation of HL60 cells into monocytes in vitro and in vivo. The expression of many proteins would have been changed during the differentiation process, and some proteins may have played key roles in the differentiation of HL60 cell line induced by this drug. Therefore, we treated HL60 cells with NSC67657 and all‐trans retinoic acid (ATRA) to identify the differentially expressed proteins and determine their functions in cellular differentiation. Of the 45 differentially expressed protein spots investigated, 24 were either elevated or decreased in both the monocytic and granulocytic differentiating HL60 cells, 8 showed significant changes only when induced by NSC67657, and 13 showed significant changes only when induced by ATRA. After verification by RT‐PCR, Western blotting, and immunocytochemistry, only the protein ICAT was found to be elevated by NSC67657 treatment alone. Although the over‐expression of ICAT is not sufficient to induce the differentiation of HL60 cells into monocytes, it did increase the proportion of CD14+ cells in cells pretreated with NSC67657. Successful application of multiple techniques including two‐dimensional gel electrophoresis, matrix‐assisted laser desorption ionization time‐of‐flight mass spectrometry, Western blotting, and eukaryotic electroporation revealed that proteomic and molecular biological analyses provide valuable tools in drug development research. Copyright © 2009 John Wiley & Sons, Ltd. 相似文献