DOCSLIB.ORG

Differential Proteomic Analysis of Human Placenta-Derived Mesenchymal Stem Cells Cultured on Normal Tissue Culture Surface and Hyaluronan-Coated Surface

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Differential Proteomic Analysis of Human Placenta-Derived Mesenchymal Stem Cells Cultured on Normal Tissue Culture Surface and Hyaluronan-Coated Surface Hindawi Publishing Corporation Stem Cells International Volume 2016, Article ID 2809192, 16 pages http://dx.doi.org/10.1155/2016/2809192 Research Article Differential Proteomic Analysis of Human Placenta-Derived Mesenchymal Stem Cells Cultured on Normal Tissue Culture Surface and Hyaluronan-Coated Surface Tzyy Yue Wong,1 Ying-Hui Chen,1 Szu-Heng Liu,1 Mairim Alexandra Solis,1 Chen-Hsiang Yu,2 Chiung-Hsin Chang,2 and Lynn L. H. Huang1,3,4,5,6 1 Institute of Biotechnology, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan 2Department of Obstetrics and Gynecology, National Cheng Kung University, Tainan 701, Taiwan 3Department of Biotechnology and Bioindustry Sciences, National Cheng Kung University, Tainan 701, Taiwan 4Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan 5Research Center of Excellence in Regenerative Medicine, National Cheng Kung University, Tainan 701, Taiwan 6Advanced Optoelectronic Technology Center, National Cheng Kung University, Tainan 701, Taiwan Correspondence should be addressed to Lynn L. H. Huang; [email protected] Received 16 May 2015; Revised 7 September 2015; Accepted 7 October 2015 Academic Editor: Andrzej Lange Copyright © 2016 Tzyy Yue Wong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Our previous results showed that hyaluronan (HA) preserved human placenta-derived mesenchymal stem cells (PDMSC) in a slow cell cycling mode similar to quiescence, the pristine state of stem cells in vivo, and HA was found to prevent murine adipose- derived mesenchymal stem cells from senescence. Here, stable isotope labeling by amino acid in cell culture (SILAC) proteomic profiling was used to evaluate the effects of HA on aging phenomenoninstemcells,comparing(1)oldandyoungpassagePDMSC cultured on normal tissue culture surface (TCS); (2) old passage on HA-coated surface (CHA) compared to TCS; (3) old and young passage on CHA. The results indicated that senescence-associated protein transgelin (TAGLN) was upregulated in old TCS. Protein CYR61, reportedly senescence-related, was downregulated in old CHA compared to old TCS. The SIRT1-interacting Nicotinamide phosphoribosyltransferase (NAMPT) increased by 2.23-fold in old CHA compared to old TCS, and is 0.48-fold lower in old TCS compared to young TCS. Results also indicated that components of endoplasmic reticulum associated degradation (ERAD) pathway were upregulated in old CHA compared to old TCS cells, potentially for overcoming stress to maintain cell function and suppress senescence. Our data points to pathways that may be targeted by HA to maintain stem cells youth. 1. Introduction towards aging. The trigger of cellular aging includes many factors, such as oxidative stress [5], genomic instability [6], Senescence is when cells reach an irreversible growth arrest altered niche microenvironment [6], altered mitochondrial [1]andisknowntoplayrolesinvariousbiologicalpro- function [7, 8], altered epigenetic regulations [9], and stem cesses such as development, apoptosis, and aging [2]. It was cells exhaustion [9]. Previous study showed that genome reviewed that mitotic cells, cells undergoing proliferation, stability such as maintained telomere length extended cell are prone to senescence [3]. Mitotic cells include stem cells, population doubling and reduced cellular aging in normal epithelial, vascular, and fibroblastic cells. The model for retinal pigment epithelial cells and foreskin fibroblasts [10]. cellular senescence first originated from Hayflick and Moor- Thus, the link between limited replicative senescence and head, who reported in 1961 that normal human diploid cells actual aging phenomenon had been established. had limited replicative lifespan [4]. Since then, senescence The known aging mechanisms include telomere shorten- is believed to play a role in two potential circumstances, ing [11], reactive oxygen species (ROS) accumulation, accu- namely, (1) to prevent tumor growth and (2) as a normal way mulated DNA damage-induced cell cycle regulation factors 2 Stem Cells International p53, p16, and p21 [3, 6], and altered cytoplasmic metabolism cultured on polystyrene tissue-culture surface were termed [12], all potentially leading to aging. The aging of stem cells TCS. leading to stem cell population decline had been suggested tooccurinthehumandiseaseknownasHutchinsonGil- 2.2. Differentiation Potential Analysis. For adipogenic dif- ford Progeria Syndrome [13]. The mesenchymal stem cells ferentiation, induction medium contained final concentra- (MSC) from aged Sprague-Dawley rats were found to have tion of 1 M dimethyl sulfoxide (DMSO; Sigma, St. Louis, compromised MSC function compared to that from young MO, USA), 0.2 mM indomethacin (Sigma, St. Louis, MO, Sprague-Dawley rats [14]. The MSC are maintained in vivo as USA), 0.5 mM 3-Isobutyl-1-methylxanthine (IBMX; Sigma, multipotent cells, capable of adipogenesis, osteogenesis, and St. Louis, MO, USA), 10 M insulin, and 10% fetal bovine chondrogenesis differentiation. Although it is well-known serum (FBS; GibcoBRL, Grand Island, NY, USA) in Dul- that stem cells are preserved in a pristine or youthful state becco’s modified Eagle’s medium high glucose medium compared to somatic cells in vivo,themechanisminvolved (DMEM; Gibco BRL, Grand Island, NY, USA). Cells were 4 2 is not fully understood. As a result, MSC are presented as a seeded at density 1×10 per cm until 100% confluence was good model for studying the aging phenomenon. reached, and medium was changed to induction medium for The goal was to study aging phenomenon using stable 4 weeks. Induction medium was changed every 72 hours. Oil isotope labeling by amino acid in cell culture (SILAC), a non- Red O (Sigma, St. Louis, MO, USA) was used to stain oil radioactive labeling method to label human placenta-derived droplets. In brief, cells were fixed in 4% paraformaldehyde, MSC (PDMSC). This study aimed to confirm the previous washed with 1x phosphate buffer saline (PBS), rinsed in results observed with hyaluronan (HA) presence. HA is a 60% isopropanol for three minutes, and stained in Oil Red major component of extracellular matrix (ECM) that belongs Ofor1hour.Afterthat,cellswerewashedusing60% to the glycosaminoglycan (GAG) family. It was observed isopropanol once, then rinsed in double-distilled water, and that HA played a role in maintaining PDMSC in slow- rinsed in 0.05% (w/v) sodium carbonate solution (Riedel-de cell cycling mode similar to stem cell quiescence [15]. HA Haen,¨ Sigma, St. Louis, MO, USA) for two minutes. Finally, induced multidrug resistance in PDMSC via CD44-PI3K- cells were counterstained with hematoxylin for one minute, Akt pathway [16]. HA was found to prevent murine adipose- washed with water, and analyzed under microscope. For derived stromal cells from senescence [17]. PDMSC of older chondrogenic differentiation, induction medium contained passage was compared to younger passage. It was found that final concentration of 6.25 g/mL insulin, 50 nM ascorbic PDMSC underwent replicative senescence after long-term in acid (JT Baker), and 10 ng/mL tumor growth factor-beta1 vitro expansion, in particular, the upregulation of proaging (TGF-1; CellGS, St. Louis, MO, USA) in DMEM high proteins and structural proteins. Molecules pertaining to glucose medium without FBS. Cells were seeded at density 1× 4 2 normal cell function maintenance such as the endoplasmic 10 per cm until 100% confluence was reached, and medium reticulum-associated degradation (ERAD) pathway during was changed to induction medium for 4 weeks. Induction stress and the COP9 signalosome-specific phosphorylation medium was changed every 72 hours. Accumulation of for p53 degradation were upregulated under HA presence glycosaminoglycan was analyzed by staining with Alcian blue compared to without HA, suggesting that the PDMSC under (Sigma, St. Louis, MO, USA). Briefly, cells were fixed in HA culture condition intended to suppress the stress of aging. 4% paraformaldehyde, washed with PBS, and incubated in 1 N hydrogen chloride (HCl; Sigma, St. Louis, MO, USA) 2. Materials and Methods solution for five minutes. Next, cells were stained with 3% Alcian blue solution in 0.1 N HCl for 30 minutes. Finally, 2.1. Cell Isolation. Full-term human placentas were obtained cellswerewashedwithwaterandanalyzedundermicroscope. from mothers at the National Cheng Kung University Osteogenesis differentiation assay was performed using the Hospital with informed consent. Procedure of the human induction medium supplemented with 10 MDMSO,10nM placenta handling and cell isolation was approved by the ascorbic acid, 10 mM 2-glycerophosphate (Sigma, St. Louis, Institutional Review Board. PDMSC were isolated based MO, USA), and 10% FBS in DMEM high glucose medium. on previous method [15]. In brief, the chorionic villi layer 1×104 2 was harvested and rinsed in Hanks’ Balanced Salt Solution Seeding cell density was per cm , and experiment (Sigma, St. Louis, MO, USA). The tissues were cut into was performed upon reaching 100% confluence. Calcification tiny pieces and digested by 347 U/mL Collagenase Type 2 was visualized after staining with Alizarin Red S (Sigma, St. ∘ (Worthington Biochemical Corporation) at 37 Cfor40min. Louis,MO,USA).Cellswerefixedin4%paraformaldehyde, The digested tissues went through filters from 500 and washed
Load more

Recommended publications
  • Critical Evaluation of Gene Expression Changes in Human Tissues In
    Supplementary Material ‘Critical Evaluation of Gene Expression Changes in Human Tissues in Response to Supplementation with Dietary Bioactive Compounds: Moving Towards Better-Quality Studies’ by Biljana Pokimica and María-Teresa García-Conesa Table S1. Characteristics of the human trials included in this review: study design, type of participants, control and intervention description, dose and duration of treatment, analyses and related bioavailability studies. Study Experimental Characteristics Reference Clinical trial Participants C (Control T (Treatment with Total daily dose, Bioavailability studies: type of sample, design (RCT, (health status, description) bioactive compounds, duration (d or h)1 compounds and (or) metabolites analysed, crossover, gender) products or diet) main results2 parallel) Mix meals and diets Persson I et al., Single arm Healthy, C: not included T: mix Veg T: 250 g, NR 2000 [1] men 21 d Møller P et al., RCT, Healthy, C1: placebo tablet + T: mix FruVeg T: 600 g, Plasma: (NS↑) β-car, T, C2 (post- vs pre-) 2003 [2] parallel, mix energy drink (same 24 d (NC) VitC, T, C2 (post- vs pre-) double blinded amount of sugars as T) (NS↓, 69%) VitC, β-car, C1 (post- vs pre-) (regarding C1 C2: tablet with and C2) antioxidants + minerals (same amount as T) + energy drink (same amount of sugars as T) Almendingen K Randomized, Healthy, C: no proper control T1,2: mix FruVeg T1: 300 g, Plasma: ↑α-car, β-car, T2 vs T1 (post-) et al., 2005 [3] crossover, mix included (comparison T2: 750 g, (NS↑) Lyc, Lut, T2 vs T1 (post-) [4] single
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Download This Article PDF Format
    Food & Function View Article Online PAPER View Journal | View Issue Human milk oligosaccharides and non-digestible carbohydrates prevent adhesion of specific Cite this: Food Funct., 2021, 12, 8100 pathogens via modulating glycosylation or inflammatory genes in intestinal epithelial cells Chunli Kong, *a,b Martin Beukema, b Min Wang,c Bart J. de Haanb and Paul de Vosb Human milk oligosaccharides (hMOs) and non-digestible carbohydrates (NDCs) are known to inhibit the adhesion of pathogens to the gut epithelium, but the mechanisms involved are not well understood. Here, the effects of 2’-FL, 3-FL, DP3–DP10, DP10–DP60 and DP30–DP60 inulins and DM7, DM55 and DM69 pectins were studied on pathogen adhesion to Caco-2 cells. As the growth phase influences viru- lence, E. coli ET8, E. coli LMG5862, E. coli O119, E. coli WA321, and S. enterica subsp. enterica LMG07233 Creative Commons Attribution-NonCommercial 3.0 Unported Licence. from both log and stationary phases were tested. Specificity for enteric pathogens was tested by including the lung pathogen K. pneumoniae LMG20218. Expression of the cell membrane glycosylation genes of galectin and glycocalyx and inflammatory genes was studied in the presence and absence of 2’-FL or NDCs. Inhibition of pathogen adhesion was observed for 2’-FL, inulins, and pectins. Pre-incubation with 2’-FL downregulated ICAM1, and pectins modified the glycosylation genes. In contrast, K. pneumoniae LMG20218 downregulated the inflammatory genes, but these were restored by pre-incubation with Received 22nd March 2021, pectins, which reduced the adhesion of K. pneumoniae LMG20218. In addition, DM69 pectin significantly Accepted 21st June 2021 upregulated the inflammatory genes.
    [Show full text]
  • Investigation of the Underlying Hub Genes and Molexular Pathogensis in Gastric Cancer by Integrated Bioinformatic Analyses
    bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Investigation of the underlying hub genes and molexular pathogensis in gastric cancer by integrated bioinformatic analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract The high mortality rate of gastric cancer (GC) is in part due to the absence of initial disclosure of its biomarkers. The recognition of important genes associated in GC is therefore recommended to advance clinical prognosis, diagnosis and and treatment outcomes. The current investigation used the microarray dataset GSE113255 RNA seq data from the Gene Expression Omnibus database to diagnose differentially expressed genes (DEGs). Pathway and gene ontology enrichment analyses were performed, and a proteinprotein interaction network, modules, target genes - miRNA regulatory network and target genes - TF regulatory network were constructed and analyzed. Finally, validation of hub genes was performed. The 1008 DEGs identified consisted of 505 up regulated genes and 503 down regulated genes.
    [Show full text]
  • Hyaluronan Synthase 3 Regulates Hyaluronan Synthesis in Cultured Human Keratinocytes
    Hyaluronan Synthase 3 Regulates Hyaluronan Synthesis in Cultured Human Keratinocytes Tetsuya Sayo, Yoshinori Sugiyama, Yoshito Takahashi, Naoko Ozawa, Shingo Sakai, Osamu Ishikawa,* Masaaki Tamura,* and Shintaro Inoue Basic Research Laboratory, Kanebo Ltd, Kanagawa, Japan; *Department of Dermatology, Gunma University School of Medicine, Gunma, Japan Three human hyaluronan synthase genes (HAS1, growth factor b downregulated HAS3 transcript HAS2, and HAS3) have been cloned, but the func- levels. The expression of HAS1 mRNA was not sig- tional differences between these HAS genes remains ni®cantly affected by either cytokine, and HAS2 obscure. The purpose of this study was to examine mRNA expression was undetectable under either which of the HAS genes are selectively regulated in basal or cytokine-stimulated conditions by northern epidermis. We examined the relation of changes blot using total RNA. Furthermore, in situ mRNA between hyaluronan production and HAS gene hybridization showed that mouse epidermal kerati- expression when cytokines were added to cultured nocytes abundantly expressed HAS3 mRNA from the human keratinocytes. Interferon-g increased hyaluro- basal to the granular cell layers, suggesting that nan production whereas transforming growth factor HAS3 functions in epidermis. These ®ndings suggest b decreased it. Both cytokines affected preferentially that HAS3 gene expression plays a crucial role in the high-molecular-mass (> 106 Da) hyaluronan produc- regulation of hyaluronan synthesis in the epidermis. tion. Consistent with the change in hyaluronan syn- Key words: HAS1/HAS2/HAS3/IFN-g/TGF-b. J Invest thesis, we found that interferon-g markedly Dermatol 118:43±48, 2002 upregulated HAS3 mRNA whereas transforming yaluronan, a high-molecular-weight linear glycosa- (Wells et al, 1991).
    [Show full text]
  • Characterization of Visceral and Subcutaneous Adipose Tissue
    J. Perinat. Med. 2016; 44(7): 813–835 Shali Mazaki-Tovi*, Adi L. Tarca, Edi Vaisbuch, Juan Pedro Kusanovic, Nandor Gabor Than, Tinnakorn Chaiworapongsa, Zhong Dong, Sonia S. Hassan and Roberto Romero* Characterization of visceral and subcutaneous adipose tissue transcriptome in pregnant women with and without spontaneous labor at term: implication of alternative splicing in the metabolic adaptations of adipose tissue to parturition DOI 10.1515/jpm-2015-0259 groups (unpaired analyses) and adipose tissue regions Received July 27, 2015. Accepted October 26, 2015. Previously (paired analyses). Selected genes were tested by quantita- published online March 19, 2016. tive reverse transcription-polymerase chain reaction. Abstract Results: Four hundred and eighty-two genes were differ- entially expressed between visceral and subcutaneous Objective: The aim of this study was to determine gene fat of pregnant women with spontaneous labor at term expression and splicing changes associated with par- (q-value < 0.1; fold change > 1.5). Biological processes turition and regions (visceral vs. subcutaneous) of the enriched in this comparison included tissue and vascu- adipose tissue of pregnant women. lature development as well as inflammatory and meta- Study design: The transcriptome of visceral and abdomi- bolic pathways. Differential splicing was found for 42 nal subcutaneous adipose tissue from pregnant women at genes [q-value < 0.1; differences in Finding Isoforms using term with (n = 15) and without (n = 25) spontaneous labor Robust Multichip Analysis scores > 2] between adipose was profiled with the Affymetrix GeneChip Human Exon tissue regions of women not in labor. Differential exon 1.0 ST array. Overall gene expression changes and the dif- usage associated with parturition was found for three ferential exon usage rate were compared between patient genes (LIMS1, HSPA5, and GSTK1) in subcutaneous tissues.
    [Show full text]
  • Figure S1. Reverse Transcription‑Quantitative PCR Analysis of ETV5 Mrna Expression Levels in Parental and ETV5 Stable Transfectants
    Figure S1. Reverse transcription‑quantitative PCR analysis of ETV5 mRNA expression levels in parental and ETV5 stable transfectants. (A) Hec1a and Hec1a‑ETV5 EC cell lines; (B) Ishikawa and Ishikawa‑ETV5 EC cell lines. **P<0.005, unpaired Student's t‑test. EC, endometrial cancer; ETV5, ETS variant transcription factor 5. Figure S2. Survival analysis of sample clusters 1‑4. Kaplan Meier graphs for (A) recurrence‑free and (B) overall survival. Survival curves were constructed using the Kaplan‑Meier method, and differences between sample cluster curves were analyzed by log‑rank test. Figure S3. ROC analysis of hub genes. For each gene, ROC curve (left) and mRNA expression levels (right) in control (n=35) and tumor (n=545) samples from The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer cohort are shown. mRNA levels are expressed as Log2(x+1), where ‘x’ is the RSEM normalized expression value. ROC, receiver operating characteristic. Table SI. Clinicopathological characteristics of the GSE17025 dataset. Characteristic n % Atrophic endometrium 12 (postmenopausal) (Control group) Tumor stage I 91 100 Histology Endometrioid adenocarcinoma 79 86.81 Papillary serous 12 13.19 Histological grade Grade 1 30 32.97 Grade 2 36 39.56 Grade 3 25 27.47 Myometrial invasiona Superficial (<50%) 67 74.44 Deep (>50%) 23 25.56 aMyometrial invasion information was available for 90 of 91 tumor samples. Table SII. Clinicopathological characteristics of The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer dataset. Characteristic n % Solid tissue normal 16 Tumor samples Stagea I 226 68.278 II 19 5.740 III 70 21.148 IV 16 4.834 Histology Endometrioid 271 81.381 Mixed 10 3.003 Serous 52 15.616 Histological grade Grade 1 78 23.423 Grade 2 91 27.327 Grade 3 164 49.249 Molecular subtypeb POLE 17 7.328 MSI 65 28.017 CN Low 90 38.793 CN High 60 25.862 CN, copy number; MSI, microsatellite instability; POLE, DNA polymerase ε.
    [Show full text]
  • Supplementary Table 1
    Supplementary Table 1. 492 genes are unique to 0 h post-heat timepoint. The name, p-value, fold change, location and family of each gene are indicated. Genes were filtered for an absolute value log2 ration 1.5 and a significance value of p ≤ 0.05. Symbol p-value Log Gene Name Location Family Ratio ABCA13 1.87E-02 3.292 ATP-binding cassette, sub-family unknown transporter A (ABC1), member 13 ABCB1 1.93E-02 −1.819 ATP-binding cassette, sub-family Plasma transporter B (MDR/TAP), member 1 Membrane ABCC3 2.83E-02 2.016 ATP-binding cassette, sub-family Plasma transporter C (CFTR/MRP), member 3 Membrane ABHD6 7.79E-03 −2.717 abhydrolase domain containing 6 Cytoplasm enzyme ACAT1 4.10E-02 3.009 acetyl-CoA acetyltransferase 1 Cytoplasm enzyme ACBD4 2.66E-03 1.722 acyl-CoA binding domain unknown other containing 4 ACSL5 1.86E-02 −2.876 acyl-CoA synthetase long-chain Cytoplasm enzyme family member 5 ADAM23 3.33E-02 −3.008 ADAM metallopeptidase domain Plasma peptidase 23 Membrane ADAM29 5.58E-03 3.463 ADAM metallopeptidase domain Plasma peptidase 29 Membrane ADAMTS17 2.67E-04 3.051 ADAM metallopeptidase with Extracellular other thrombospondin type 1 motif, 17 Space ADCYAP1R1 1.20E-02 1.848 adenylate cyclase activating Plasma G-protein polypeptide 1 (pituitary) receptor Membrane coupled type I receptor ADH6 (includes 4.02E-02 −1.845 alcohol dehydrogenase 6 (class Cytoplasm enzyme EG:130) V) AHSA2 1.54E-04 −1.6 AHA1, activator of heat shock unknown other 90kDa protein ATPase homolog 2 (yeast) AK5 3.32E-02 1.658 adenylate kinase 5 Cytoplasm kinase AK7
    [Show full text]
  • Resveratrol Inhibits Cell Cycle Progression by Targeting Aurora Kinase a and Polo-Like Kinase 1 in Breast Cancer Cells
    3696 ONCOLOGY REPORTS 35: 3696-3704, 2016 Resveratrol inhibits cell cycle progression by targeting Aurora kinase A and Polo-like kinase 1 in breast cancer cells RUBICELI MEDINA-AGUILAR1, LAURENCE A. Marchat2, ELENA ARECHAGA OCAMPO3, Patricio GARIGLIO1, JAIME GARCÍA MENA1, NICOLÁS VILLEGAS SEPÚlveda4, MACARIO MartÍNEZ CASTILLO4 and CÉSAR LÓPEZ-CAMARILLO5 1Department of Genetics and Molecular Biology, CINVESTAV-IPN, Mexico D.F.; 2Molecular Biomedicine Program and Biotechnology Network, National School of Medicine and Homeopathy, National Polytechnic Institute, Mexico D.F.; 3Natural Sciences Department, Metropolitan Autonomous University, Mexico D.F.; 4Department of Molecular Biomedicine, CINVESTAV-IPN, Mexico D.F.; 5Oncogenomics and Cancer Proteomics Laboratory, Universidad Autónoma de la Ciudad de México, Mexico D.F., Mexico Received December 4, 2015; Accepted January 8, 2016 DOI: 10.3892/or.2016.4728 Abstract. The Aurora protein kinase (AURKA) and the MDA-MB-231 and MCF-7 cells. By western blot assays, we Polo-like kinase-1 (PLK1) activate the cell cycle, and they confirmed that resveratrol suppressed AURKA, CCND1 and are considered promising druggable targets in cancer CCNB1 at 24 and 48 h. In summary, we showed for the first time therapy. However, resistance to chemotherapy and to specific that resveratrol regulates cell cycle progression by targeting small-molecule inhibitors is common in cancer patients; thus AURKA and PLK1. Our findings highlight the potential use of alternative therapeutic approaches are needed to overcome resveratrol as an adjuvant therapy for breast cancer. clinical resistance. Here, we showed that the dietary compound resveratrol suppressed the cell cycle by targeting AURKA Introduction and PLK1 kinases. First, we identified genes modulated by resveratrol using a genome-wide analysis of gene expression Cancer development results from the interaction between in MDA-MB-231 breast cancer cells.
    [Show full text]
  • Mechanical Stress Induce PG-E2 in Murine Synovial Fibroblasts Originating from the Temporomandibular Joint
    cells Article Mechanical Stress Induce PG-E2 in Murine Synovial Fibroblasts Originating from the Temporomandibular Joint Ute Nazet 1,* , Laura Feulner 1, Dominique Muschter 2 , Patrick Neubert 3, Valentin Schatz 3, Susanne Grässel 2 , Jonathan Jantsch 3, Peter Proff 1, Agnes Schröder 1,† and Christian Kirschneck 1,† 1 Department of Orthodontics, University Medical Centre of Regensburg, D-93053 Regensburg, Germany; [email protected] (L.F.); [email protected] (P.P.); [email protected] (A.S.); [email protected] (C.K.) 2 Centre for Medical Biotechnology, Department of Orthopaedic Surgery, Experimental Orthopaedics, University of Regensburg, D-93053 Regensburg, Germany; [email protected] (D.M.); [email protected] (S.G.) 3 Institute of Clinical Microbiology and Hygiene, University Hospital of Regensburg, D-93053 Regensburg, Germany; [email protected] (P.N.); [email protected] (V.S.); [email protected] (J.J.) * Correspondence: [email protected]; Tel.: +49-941-944-4990 † Contributed equally. Abstract: Genetic predisposition, traumatic events, or excessive mechanical exposure provoke arthritic changes in the temporomandibular joint (TMJ). We analysed the impact of mechanical stress that might be involved in the development and progression of TMJ osteoarthritis (OA) on murine synovial fibroblasts (SFs) of temporomandibular origin. SFs were subjected to different Citation: Nazet, U.; Feulner, L.; Muschter, D.; Neubert, P.; Schatz, V.; protocols of mechanical stress, either to a high-frequency tensile strain for 4 h or to a tensile strain of Grässel, S.; Jantsch, J.; Proff, P.; varying magnitude for 48 h. The TMJ OA induction was evaluated based on the gene and protein Schröder, A.; Kirschneck, C.
    [Show full text]
  • Molecular Signatures Differentiate Immune States in Type 1 Diabetes Families
    Page 1 of 65 Diabetes Molecular signatures differentiate immune states in Type 1 diabetes families Yi-Guang Chen1, Susanne M. Cabrera1, Shuang Jia1, Mary L. Kaldunski1, Joanna Kramer1, Sami Cheong2, Rhonda Geoffrey1, Mark F. Roethle1, Jeffrey E. Woodliff3, Carla J. Greenbaum4, Xujing Wang5, and Martin J. Hessner1 1The Max McGee National Research Center for Juvenile Diabetes, Children's Research Institute of Children's Hospital of Wisconsin, and Department of Pediatrics at the Medical College of Wisconsin Milwaukee, WI 53226, USA. 2The Department of Mathematical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53211, USA. 3Flow Cytometry & Cell Separation Facility, Bindley Bioscience Center, Purdue University, West Lafayette, IN 47907, USA. 4Diabetes Research Program, Benaroya Research Institute, Seattle, WA, 98101, USA. 5Systems Biology Center, the National Heart, Lung, and Blood Institute, the National Institutes of Health, Bethesda, MD 20824, USA. Corresponding author: Martin J. Hessner, Ph.D., The Department of Pediatrics, The Medical College of Wisconsin, Milwaukee, WI 53226, USA Tel: 011-1-414-955-4496; Fax: 011-1-414-955-6663; E-mail: [email protected]. Running title: Innate Inflammation in T1D Families Word count: 3999 Number of Tables: 1 Number of Figures: 7 1 For Peer Review Only Diabetes Publish Ahead of Print, published online April 23, 2014 Diabetes Page 2 of 65 ABSTRACT Mechanisms associated with Type 1 diabetes (T1D) development remain incompletely defined. Employing a sensitive array-based bioassay where patient plasma is used to induce transcriptional responses in healthy leukocytes, we previously reported disease-specific, partially IL-1 dependent, signatures associated with pre and recent onset (RO) T1D relative to unrelated healthy controls (uHC).
    [Show full text]
  • Glycan Metabolism a Validated Grna Library for CRISPR/Cas9
    Glycobiology, 2018, vol. 28, no. 5, 295–305 doi: 10.1093/glycob/cwx101 Advance Access Publication Date: 5 January 2018 Original Article Glycan Metabolism A validated gRNA library for CRISPR/Cas9 targeting of the human glycosyltransferase Downloaded from https://academic.oup.com/glycob/article-abstract/28/5/295/4791732 by guest on 08 October 2018 genome Yoshiki Narimatsu2,3,1, Hiren J Joshi2, Zhang Yang2,3, Catarina Gomes2,4, Yen-Hsi Chen2, Flaminia C Lorenzetti 2, Sanae Furukawa2, Katrine T Schjoldager2, Lars Hansen2, Henrik Clausen2, Eric P Bennett2,1, and Hans H Wandall2 2Copenhagen Center for Glycomics, Departments of Cellular and Molecular Medicine and Odontology, Faculty of Health Sciences, University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark, 3GlycoDisplay Aps, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark, and 4Instituto de Investigação e Inovação em Saúde,i3S; Institute of Molecular Pathology and Immunology of University of Porto, Ipatimup, Rua Júlio Amaral de Carvalho, 45, Porto 4200-135, Portugal 1To whom correspondence should be addressed: Tel: +45-35335528; Fax: +45-35367980; e-mail: [email protected] (Y.N.); Tel: +4535326630; Fax: +45-35367980; e-mail: [email protected] (E.P.B.) Received 25 September 2017; Revised 20 November 2017; Editorial decision 5 December 2017; Accepted 7 December 2017 Abstract Over 200 glycosyltransferases are involved in the orchestration of the biosynthesis of the human glycome, which is comprised of all glycan structures found on different glycoconjugates in cells. The glycome is vast, and despite advancements in analytic strategies it continues to be difficult to decipher biological roles of glycans with respect to specific glycan structures, type of glycoconju- gate, particular glycoproteins, and distinct glycosites on proteins.
    [Show full text]