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‣ Expression of Homeobox Genes in Oral Squamous Cell Carcinoma Cell Lines Treated With All-Trans Retinoic Acid

ACQUAFREDA, Thais; NUNES, Fabio Daumas; SOPRANO, Dianne Robert; SOPRANO, Kenneth J.
Fonte: WILEY-LISS Publicador: WILEY-LISS
Tipo: Artigo de Revista Científica
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Oral squamous cell carcinoma (OSCC) may arise from potentially malignant oral lesions. All-trans retinoic acid (atRA), which plays a role in cell growth and differentiation, has been studied as a possible chemotherapeutic agent in the prevention of this progression. While the mechanism by which atRA suppresses cell growth has not been completely elucidated, it is known that homeobox genes are atRA targets. To determine if these genes are involved in the atRA-mediated OSCC growth inhibition, PCR array was performed to evaluate the expression of 84 homeobox genes in atRA-sensitive SCC-25 cells compared to atRA-resistant SCC-9 cells following 7 days with atRA treatment. Results showed that the expression of 8 homeobox genes was downregulated and expression of 4 was upregulated in SCC-25 cells but not in SCC-9 cells. Gene expression levels were confirmed for seven of these genes by RT-qPCR. Expression of three genes that showed threefold downregulation was evaluated in SCC-25 cells treated with atRA for 3, 5, and 7 days. Three different patterns of atRA-dependent gene expression were observed. ALX1 showed downregulation only on day 7. DLX3 showed reduced expression on day 3 and further reduced on clay 7. TLX1 showed downregulation only on days 5 and 7. Clearly the expression of homeobox genes is modulated by atRA in OSCC cell lines. However...

‣ Targeted Comparative RNA Interference Analysis Reveals Differential Requirement of Genes Essential for Cell Proliferation

Machida, Yuichi J.; Chen, Yuefeng; Machida, Yuka; Malhotra, Ankit; Sarkar, Sukumar; Dutta, Anindya
Fonte: The American Society for Cell Biology Publicador: The American Society for Cell Biology
Tipo: Artigo de Revista Científica
Publicado em /11/2006 Português
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Differences in the genetic and epigenetic make up of cell lines have been very useful for dissecting the roles of specific genes in the biology of a cell. Targeted comparative RNAi (TARCOR) analysis uses high throughput RNA interference (RNAi) against a targeted gene set and rigorous quantitation of the phenotype to identify genes with a differential requirement for proliferation between cell lines of different genetic backgrounds. To demonstrate the utility of such an analysis, we examined 257 growth-regulated genes in parallel in a breast epithelial cell line, MCF10A, and a prostate cancer cell line, PC3. Depletion of an unexpectedly high number of genes (25%) differentially affected proliferation of the two cell lines. Knockdown of many genes that spare PC3 (p53−) but inhibit MCF10A (p53+) proliferation induces p53 in MCF10A cells. EBNA1BP2, involved in ribosome biogenesis, is an example of such a gene, with its depletion arresting MCF10A at G1/S in a p53-dependent manner. TARCOR is thus useful for identifying cell type–specific genes and pathways involved in proliferation and also for exploring the heterogeneity of cell lines. In particular, our data emphasize the importance of considering the genetic status, when performing siRNA screens in mammalian cells.

‣ Inflammatory Levels of Nitric Oxide Inhibit Airway Epithelial Cell Migration by Inhibition of the Kinase ERK1/2 and Activation of Hypoxia-inducible Factor-1α*S⃞

Bove, Peter F.; Hristova, Milena; Wesley, Umadevi V.; Olson, Nels; Lounsbury, Karen M.; van der Vliet, Albert
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
Publicado em 27/06/2008 Português
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Increased synthesis of NO during airway inflammation, caused by induction of nitric-oxide synthase 2 in several lung cell types, may contribute to epithelial injury and permeability. To investigate the consequence of elevated NO production on epithelial function, we exposed cultured monolayers of human bronchial epithelial cells to the NO donor diethylenetriaamine NONOate. At concentrations generating high nanomolar levels of NO, representative of inflammatory conditions, diethylenetriaamine NONOate markedly reduced wound closure in an in vitro scratch injury model, primarily by inhibiting epithelial cell migration. Analysis of signaling pathways and gene expression profiles indicated a rapid induction of the mitogen-activated protein kinase phosphatase (MPK)-1 and decrease in extracellular signal-regulated kinase (ERK)1/2 activation, as well as marked stabilization of hypoxia-inducible factor (HIF)-1α and activation of hypoxia-responsive genes, under these conditions. Inhibition of ERK1/2 signaling using U0126 enhanced HIF-1α stabilization, implicating ERK1/2 dephosphorylation as a contributing mechanism in NO-mediated HIF-1α activation. Activation of HIF-1α by the hypoxia mimic cobalt chloride, or cell transfection with a degradation-resistant HIF-1α mutant construct inhibited epithelial wound repair...

‣ Host Cell Autophagy Is Induced by Toxoplasma gondii and Contributes to Parasite Growth*

Wang, Yubao; Weiss, Louis M.; Orlofsky, Amos
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
Publicado em 16/01/2009 Português
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Autophagy has been shown to contribute to defense against intracellular bacteria and parasites. In comparison, the ability of such pathogens to manipulate host cell autophagy to their advantage has not been examined. Here we present evidence that infection by Toxoplasma gondii, an intracellular protozoan parasite, induces host cell autophagy in both HeLa cells and primary fibroblasts, via a mechanism dependent on host Atg5 but independent of host mammalian target of rapamycin suppression. Infection led to the conversion of LC3 to the autophagosome-associated form LC3-II, to the accumulation of LC3-containing vesicles near the parasitophorous vacuole, and to the relocalization toward the vacuole of structures labeled by the phosphatidylinositol 3-phosphate indicator YFP-2×FYVE. The autophagy regulator beclin 1 was concentrated in the vicinity of the parasitophorous vacuole in infected cells. Inhibitor studies indicated that parasite-induced autophagy is dependent on calcium signaling and on abscisic acid. At physiologically relevant amino acid levels, parasite growth became defective in Atg5-deficient cells, indicating a role for host cell autophagy in parasite recovery of host cell nutrients. A flow cytometric analysis of cell size as a function of parasite content revealed that autophagy-dependent parasite growth correlates with autophagy-dependent consumption of host cell mass that is dependent on parasite progression. These findings indicate a new role for autophagy as a pathway by which parasites may effectively compete with the host cell for limiting anabolic resources.

‣ Zinc Finger Transcription Factor INSM1 Interrupts Cyclin D1 and CDK4 Binding and Induces Cell Cycle Arrest*

Zhang, Tao; Liu, Wei-Dong; Saunee, Nicolle A.; Breslin, Mary B.; Lan, Michael S.
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
Publicado em 27/02/2009 Português
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INSM1 is a zinc finger transcription factor that plays an important role in pancreatic β-cell development. To further evaluate its role in cell fate determination, we investigated INSM1 effects on cell cycle function. The cyclin box of cyclin D1 is essential for INSM1 binding. Competitive pull-down and co-immunoprecipitation revealed that INSM1 binding to cyclin D1 interrupts its association with CDK4 and induces hypophosphorylation of the retinoblastoma protein. An inducible Tet-on system was established in Cos-7 and Panc-1 cells. Using serum starvation, we synchronized the cell cycle and subsequently induced cell cycle progression by serum stimulation. Comparison of the INSM1 induction group with the noninduced control group, INSM1 ectopic expression causes cell cycle arrest, whereas the INSM1-mediated cell cycle arrest could be reversed by cyclin D1 and CDK4 overexpression. The proline-rich N-terminal portion of INSM1 is required for cyclin D1 binding. Mutation of proline residues abolished cyclin D1 binding and also diminished its ability to induce cell cycle arrest. Cellular proliferation of Panc-1 cells was inhibited by INSM1 overexpression demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay...

‣ Krüppel-like Factor 5 Shows Proliferation-specific Roles in Vascular Remodeling, Direct Stimulation of Cell Growth, and Inhibition of Apoptosis*

Suzuki, Toru; Sawaki, Daigo; Aizawa, Kenichi; Munemasa, Yoshiko; Matsumura, Takayoshi; Ishida, Junichi; Nagai, Ryozo
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
Publicado em 03/04/2009 Português
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Krüppel-like factor 5 (KLF5), originally isolated as a regulator of phenotypic modulation of vascular smooth muscle cells, induces pathological cell growth and is expressed in the neointima. Although induction of KLF5 up-regulates growth factors like platelet-derived growth factor-A chain, how KLF5 actually contributes to vascular remodeling, notably its direct effects on cell proliferation, had been poorly clarified. To investigate the effects of KLF5 on neointimal formation, we at first performed adenoviral overexpression of KLF5 to rats subjected to carotid balloon injury. Neointimal formation and proliferating cell nuclear antigen-positive rate were significantly increased at 14 days after injury in the KLF5-treated animals. At the cellular level, overexpression of KLF5 also resulted in markedly increased cell proliferation and cell cycle progression. As a molecular mechanism, we showed that KLF5 directly bound to the promoter and up-regulated gene expression of cyclin D1, as well as showing specific transactivation of cyclins and cyclin-dependent kinase inhibitors in cardiovascular cells. Conversely, knockdown of KLF5 by RNA interference specifically down-regulated cyclin D1 and impaired vascular smooth muscle cell proliferation. Furthermore...

‣ Differential Regulation of Cell Type-specific Apoptosis by Stromelysin-3: A POTENTIAL MECHANISM VIA THE CLEAVAGE OF THE LAMININ RECEPTOR DURING TAIL RESORPTION IN XENOPUS LAEVIS*

Mathew, Smita; Fu, Liezhen; Fiorentino, Maria; Matsuda, Hiroki; Das, Biswajit; Shi, Yun-Bo
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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Matrix metalloproteinases (MMPs) have been extensively studied because of their functional attributes in development and diseases. However, relatively few in vivo functional studies have been reported on the roles of MMPs in postembryonic organ development. Amphibian metamorphosis is a unique model for studying MMP function during vertebrate development because of its dependence on thyroid hormone (T3) and the ability to easily manipulate this process with exogenous T3. The MMP stromelysin-3 (ST3) is induced by T3, and its expression correlates with cell death during metamorphosis. We have previously shown that ST3 is both necessary and sufficient for larval epithelial cell death in the remodeling intestine. To investigate the roles of ST3 in other organs and especially on different cell types, we have analyzed the effect of transgenic overexpression of ST3 in the tail of premetamorphic tadpoles. We report for the first time that ST3 expression, in the absence of T3, caused significant muscle cell death in the tail of premetamorphic transgenic tadpoles. On the other hand, only relatively low levels of epidermal cell death were induced by precocious ST3 expression in the tail, contrasting what takes place during natural and T3-induced metamorphosis when ST3 expression is high. This cell type-specific apoptotic response to ST3 in the tail suggests distinct mechanisms regulating cell death in different tissues. Furthermore...

‣ LFA-1 and CD2 Synergize for the Erk1/2 Activation in the Natural Killer (NK) Cell Immunological Synapse*

Zheng, Xiaodong; Wang, Yanyan; Wei, Haiming; Sun, Rui; Tian, Zhigang
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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Natural killer (NK) cell recognition and formation of a conjugate with target cells, followed by intracellular signal pathway activation and degradation of cytolytic granules, are essential for NK cell cytotoxicity. In this study, NK92 cells were used to investigate synapse formation and subsequent signaling after binding to the target cell. The binding rate of the NK92-target cell was associated with NK92 cell cytotoxicity. Confocal results showed that adhesion molecules, LFA-1 (CD11a) and CD2, accumulated at the interface of the NK92-K562 contact. Ligation with K562 cells activated the Erk1/2 signal pathway of NK92 cells. The blocking of the NK-target conjugate by EDTA or anti-CD11a or/and anti-CD2 antibody decreased the phosphorylation of Erk1/2 and NK cell cytotoxicity. Inhibition of Erk1/2 phosphorylation by the chemical inhibitor U0126 suppressed the cytolytic activity of NK92 cells, but had no effect on NK-target conjugate formation. Thus, conjugate formation of the NK92-target cell was prerequisite to NK cell activation, and subsequent signal transduction was also required for NK cell cytotoxicity.

‣ NDRG4 Is Required for Cell Cycle Progression and Survival in Glioblastoma Cells*

Schilling, Stephen H.; Hjelmeland, Anita B.; Radiloff, Daniel R.; Liu, Irwin M.; Wakeman, Timothy P.; Fielhauer, Jeffrey R.; Foster, Erika H.; Lathia, Justin D.; Rich, Jeremy N.; Wang, Xiao-Fan; Datto, Michael B.
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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NDRG4 is a largely unstudied member of the predominantly tumor suppressive N-Myc downstream-regulated gene (NDRG) family. Unlike its family members NDRG1–3, which are ubiquitously expressed, NDRG4 is expressed almost exclusively in the heart and brain. Given this tissue-specific expression pattern and the established tumor suppressive roles of the NDRG family in regulating cellular proliferation, we investigated the cellular and biochemical functions of NDRG4 in the context of astrocytes and glioblastoma multiforme (GBM) cells. We show that, in contrast to NDRG2, NDRG4 expression is elevated in GBM and NDRG4 is required for the viability of primary astrocytes, established GBM cell lines, and both CD133+ (cancer stem cell (CSC)-enriched) and CD133− primary GBM xenograft cells. While NDRG4 overexpression has no effect on cell viability, NDRG4 knockdown causes G1 cell cycle arrest followed by apoptosis. The initial G1 arrest is associated with a decrease in cyclin D1 expression and an increase in p27Kip1 expression, and the subsequent apoptosis is associated with a decrease in the expression of XIAP and survivin. As a result of these effects on cell cycle progression and survival, NDRG4 knockdown decreases the tumorigenic capacity of established GBM cell lines and GBM CSC-enriched cells that have been implanted intracranially into immunocompromised mice. Collectively...

‣ The Hexosamine Biosynthesis Pathway Is Essential for Pancreatic Beta Cell Development*

Filhoulaud, Gaëlle; Guillemain, Ghislaine; Scharfmann, Raphaël
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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Pancreatic exocrine and endocrine cells develop during embryonic life from endodermal progenitors. This process depends on activation of a hierarchy of transcription factors. Although information is available regarding the mesodermal signals controlling pancreas development, little is known about the role of environmental factors such as nutrients, including glucose, that also may impact development. Previously, we showed that glucose plays an important and specific role in beta cell development by activating the transition of Neurogenin3-positive endocrine progenitors into beta cells. Here, we examined the implication of glucose metabolism and more precisely the role of the hexosamine biosynthesis pathway (HBP) to understand the mechanisms by which glucose regulates beta cell development. We have established an in vitro model of endocrine and exocrine cells development from embryonic day 13.5 rat pancreases in a manner that replicates in vivo pancreas development perfectly. Using this model, we tested the effect of selective inhibitors and activators of the HBP and found that the HBP has a modest effect on cell proliferation and exocrine cell differentiation. On the other hand, beta cell development is tightly controlled by the HBP. Specifically...

‣ A Biologically Active Sequence of the Laminin α2 Large Globular 1 Domain Promotes Cell Adhesion through Syndecan-1 by Inducing Phosphorylation and Membrane Localization of Protein Kinase Cδ*

Jung, Sung Youn; Kim, Jin-Man; Kang, Hyun Ki; Jang, Da Hyun; Min, Byung-Moo
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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Laminin-2 promotes basement membrane assembly and peripheral myelinogenesis; however, a receptor-binding motif within laminin-2 and the downstream signaling pathways for motif-mediated cell adhesion have not been fully established. The human laminin-2 α2 chain cDNAs cloned from human keratinocytes and fibroblasts correspond to the laminin α2 chain variant sequence from the human brain. Individually expressed recombinant large globular (LG) 1 protein promotes cell adhesion and has heparin binding activities. Studies with synthetic peptides delineate the DLTIDDSYWYRI motif (Ln2-P3) within the LG1 as a major site for both heparin and cell binding. Cell adhesion to LG1 and Ln2-P3 is inhibited by treatment of heparitinase I and chondroitinase ABC. Syndecan-1 from PC12 cells binds to LG1 and Ln2-P3 and colocalizes with both molecules. Suppression of syndecan-1 with RNA interference inhibits cell adhesion to LG1 and Ln2-P3. The binding of syndecan-1 with LG1 and Ln2-P3 induces the recruitment of protein kinase Cδ (PKCδ) into the membrane and stimulates its tyrosine phosphorylation. A decrease in PKCδ activity significantly reduces cell adhesion to LG1 and Ln2-P3. Taken together, these results indicate that the Ln2-P3 motif and LG1 domain...

‣ Non-canonical Wnt Signaling Induces Ubiquitination and Degradation of Syndecan4

Carvallo, Loreto; Muñoz, Rosana; Bustos, Francisco; Escobedo, Noelia; Carrasco, Héctor; Olivares, Gonzalo; Larraín, Juan
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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Dynamic regulation of cell adhesion receptors is required for proper cell migration in embryogenesis, tissue repair, and cancer. Integrins and Syndecan4 (SDC4) are the main cell adhesion receptors involved in focal adhesion formation and are required for cell migration. SDC4 interacts biochemically and functionally with components of the Wnt pathway such as Frizzled7 and Dishevelled. Non-canonical Wnt signaling, particularly components of the planar cell polarity branch, controls cell adhesion and migration in embryogenesis and metastasic events. Here, we evaluate the effect of this pathway on SDC4. We have found that Wnt5a reduces cell surface levels and promotes ubiquitination and degradation of SDC4 in cell lines and dorsal mesodermal cells from Xenopus gastrulae. Gain- and loss-of-function experiments demonstrate that Dsh plays a key role in regulating SDC4 steady-state levels. Moreover, a SDC4 deletion construct that interacts inefficiently with Dsh is resistant to Wnt5a-induced degradation. Non-canonical Wnt signaling promotes monoubiquitination of the variable region of SDC4 cytoplasmic domain. Mutation of these specific residues abrogates ubiquitination and results in increased SDC4 steady-state levels. This is the first example of a cell surface protein ubiquitinated and degraded in a Wnt/Dsh-dependent manner.

‣ Sources of Cell-to-cell Variability in Canonical Nuclear Factor-κB (NF-κB) Signaling Pathway Inferred from Single Cell Dynamic Images*

Kalita, Mridul K.; Sargsyan, Khachik; Tian, Bing; Paulucci-Holthauzen, Adriana; Najm, Habib N.; Debusschere, Bert J.; Brasier, Allan R.
Fonte: American Society for Biochemistry and Molecular Biology Publicador: American Society for Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
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The canonical nuclear factor-κB (NF-κB) signaling pathway controls a gene network important in the cellular inflammatory response. Upon activation, NF-κB/RelA is released from cytoplasmic inhibitors, from where it translocates into the nucleus, subsequently activating negative feedback loops producing either monophasic or damped oscillatory nucleo-cytoplasmic dynamics. Although the population behavior of the NF-κB pathway has been extensively modeled, the sources of cell-to-cell variability are not well understood. We describe an integrated experimental-computational analysis of NF-κB/RelA translocation in a validated cell model exhibiting monophasic dynamics. Quantitative measures of cellular geometry and total cytoplasmic concentration and translocated RelA amounts were used as priors in Bayesian inference to estimate biophysically realistic parameter values based on dynamic live cell imaging studies of enhanced GFP-tagged RelA in stable transfectants. Bayesian inference was performed on multiple cells simultaneously, assuming identical reaction rate parameters, whereas cellular geometry and initial and total NF-κB concentration-related parameters were cell-specific. A subpopulation of cells exhibiting distinct kinetic profiles was identified that corresponded to differences in the IκBα translation rate. We conclude that cellular geometry...

‣ The cell biology of lignification in higher plants

Barros, Jaime; Serk, Henrik; Granlund, Irene; Pesquet, Edouard
Fonte: Oxford University Press Publicador: Oxford University Press
Tipo: Artigo de Revista Científica Formato: text/html
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Background Lignin is a polyphenolic polymer that strengthens and waterproofs the cell wall of specialized plant cell types. Lignification is part of the normal differentiation programme and functioning of specific cell types, but can also be triggered as a response to various biotic and abiotic stresses in cells that would not otherwise be lignifying. Scope Cell wall lignification exhibits specific characteristics depending on the cell type being considered. These characteristics include the timing of lignification during cell differentiation, the palette of associated enzymes and substrates, the sub-cellular deposition sites, the monomeric composition and the cellular autonomy for lignin monomer production. This review provides an overview of the current understanding of lignin biosynthesis and polymerization at the cell biology level. Conclusions The lignification process ranges from full autonomy to complete co-operation depending on the cell type. The different roles of lignin for the function of each specific plant cell type are clearly illustrated by the multiple phenotypic defects exhibited by knock-out mutants in lignin synthesis, which may explain why no general mechanism for lignification has yet been defined. The range of phenotypic effects observed include altered xylem sap transport...

‣ Mechanisms of homotypic lymphocyte aggregation and cell motility characteristics induced by activation of VLA integrins

Neelamegham, Sriram
Fonte: Universidade Rice Publicador: Universidade Rice
Tipo: Thesis; Text Formato: 182 p.; application/pdf
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Cell Adhesion may be modulated at the plasma membrane by intracellular signals or antibodies which confer an active ligand-binding conformation. Lymphocyte homotypic aggregation measured in tissue culture constitutes a model system in which to study the mechanism of $\beta\sb1$ integrin dependent function. First, a quantitative assay for homotypic cellular aggregation has been described. This procedure applies a digital image analysis technique to measure aggregation kinetics both in terms of evolution of aggregate size and changes in cell stacking. The method allows us to automate the image processing and data analysis steps in order to minimize user intervention and to improve the reproducibility of the measurements. Second, we studied the mechanism of homotypic aggregation induced by various monoclonal antibodies to the $\beta\sb1$ integrin. Our findings indicate that the rate and extent of adhesion in Jurkat cells can be modulated by the stoichiometry of sites occupied by the aggregation inducing antibody, 33B6, and the inhibiting antibody, 18D3. We also hypothesize that homotypic aggregation is induced by a change in the conformation of the $\beta\sb1$ integrin. Further, this conformation of the VLA integrin mediating aggregation is novel and distinct from the conformation recognized by mAb 15/7 which supports cell binding to VCAM-1 and fibronectin. Third...

‣ Los mapas conceptuales como estrategia didáctica para el aprendizaje de conceptos de biología celular en estudiantes de ciencias de la salud / Concept maps as a didactic strategy for learning of concepts of cell biology in students of health sciences

Danilo Lusbin Ariza Rúa; Universidad Tecnológica de Bolívar; Iván Antonio Yaber Goenaga; Universidad Tecnológica de Bolívar; Jorge Luis Muñiz; Universidad Tecnológica de Bolívar; Julio Seferino Hurtado Márquez; Universidad Tecnológica de Bolív
Fonte: Universidad del Norte Publicador: Universidad del Norte
Tipo: article; publishedVersion Formato: application/pdf
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ResumenPara los estudiantes de ciencias de la salud, el conocimiento de la biología constituye un pilar fundamental para afrontar con éxito los problemas que se les presenten relacionados con este campo del conocimiento y para interpretar los fenómenos concretos de las ciencias médicas y de la salud. Este artículo muestra los resultados del uso de los mapas conceptuales para el aprendizaje significativo de conceptos de biología celular.Objetivo: Determinar la efectividad de los mapas conceptuales como estrategia didáctica en el aprendizaje de conceptos de biología celular en estudiantes de ciencias de la salud.Materiales y métodos. Se trabajó un diseño cuasiexperimental pretest postest con dos grupos intactos: un grupo experimental (usó los mapas conceptuales como estrategia de aprendizaje) y un grupo control (no usó los mapas conceptuales como estrategia de aprendizaje). Los estudiantes fueron evaluados con preguntas de selección múltiple con única respuesta, en los niveles de conocimiento, comprensión y aplicación del dominio cognitivo de la Taxonomía de Bloom.Resultados: En el postest no se hallaron diferencias significativas en el total de preguntas. Sin embargo, se encontraron diferencias significativas entre los grupos en el nivel de aplicación...

‣ Stem and progenitor cell division kinetics during postnatal mouse mammary gland development

Giraddi, Rajshekhar R.; Shehata, Mona; Gallardo, Mercedes; Blasco, Maria A.; Simons, Benjamin D.; Stingl, John
Fonte: NPG Publicador: NPG
Tipo: Article; published version
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This is the final version of the article. It was first available from Nature via http://dx.doi.org/10.1038/ncomms9487; The cycling properties of mammary stem and progenitor cells is not well understood. To determine the division properties of these cells, we administered synthetic nucleosides for varying periods of time to mice at different stages of postnatal development and monitored the rate of uptake of these nucleosides in the different mammary cell compartments. Here we show that most cell division in the adult virgin gland is restricted to the oestrogen receptor-expressing luminal cell lineage. Our data also demonstrate that the oestrogen receptor-expressing, milk and basal cell subpopulations have telomere lengths and cell division kinetics that are not compatible with these cells being hierarchically organized; instead, our data indicate that in the adult homeostatic gland, each cell type is largely maintained by its own restricted progenitors. We also observe that transplantable stem cells are largely quiescent during oestrus, but are cycling during dioestrus when progesterone levels are high.; We thank the members of Stingl lab, Doug Winton, Jason Carroll, Robert Clarke, Phil Jones and Hamid Raza Ali for scientific discussions. We thank the core facilities at the Cancer Research UK-CI for enabling experiments. In particular...

‣ Regulation of Mitochondrial Dynamics during Apoptosis and the Cell Cycle

Horn, Sarah R.
Fonte: Universidade Duke Publicador: Universidade Duke
Tipo: Dissertação Formato: 2600492 bytes; application/pdf
Publicado em //2010 Português
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Homeostatic maintenance of cellular mitochondria requires a dynamic balance between fission and fusion, and disruptions in this balance have been implicated in multiple pathological conditions, including Charcot-Marie-Tooth, Parkinson's, and Alzheimer's diseases. Whereas deregulated fission and fusion can be detrimental to health and survival, controlled changes in morphology are important for processes like cellular division and apoptosis. Specifically, regulated mitochondrial fission occurs closely with cytochrome c release during apoptosis and upon entry into mitosis during the cell cycle. Using cell culture-based assays, microscopy, and fly genetics, we examine how changes in the mitochondrial network are mediated at the molecular level during apoptosis and the cell cycle.

First, we report that the fly protein Reaper induces mitochondrial fragmentation in mammalian cells, likely through inhibition of the mitochondrial fusion protein Mfn2. Reaper colocalizes with and binds to Mfn2 and its fly orthologue dMFN, and the colocalization of the two proteins is necessary for Reaper-induced mitochondrial fission. Moreover, the overexpression of dMFN inhibits Reaper-induced killing both in vitro and in vivo.

Our data and work in a number of experimental systems demonstrate a requirement for mitochondrial fragmentation during apoptosis that is conserved from worms to flies to mammals. Our findings indicate that Reaper may function to inactivate mitochondrial metabolic function and/or to facilitate mitochondrial elimination during apoptosis.

Secondly...

‣ Tracing blastomere fate choices of early embryos in single cell culture

Yunhan Hong; Haobin Zhao; Ni Hong; Zhendong Li; Meisheng Yi; Rong Liu; Mingyou Li; Yan Yan; Yongming Yuan; Chang Ming Li; Ruowen Ge; Jianxin Song
Fonte: Nature Preceedings Publicador: Nature Preceedings
Tipo: Manuscript
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Blastomeres of early vertebrate embryos undergo numerous fate choices for division, motility, pluripotency maintenance and restriction culminating in various cell lineages. Tracing blastomere fate choices at the single cell level in vitro has not been possible because of the inability to isolate and cultivate early blastomeres as single cells. Here we report the establishment of single cell culture system in the fish medaka, enabling the isolation and cultivation of individual blastomeres from 16- to 64-cell embryos for fate tracing at the single cell level in vitro. Interestingly, these blastomeres immediately upon isolation exhibit motility, lose synchronous divisions and even stop dividing in ≥50% cases, suggesting that the widely accepted nucleocytoplasmic ratio controlling synchronous divisions in entire embryos does not operate on individual blastomeres. We even observed abortive division, endomitosis and cell fusion. Strikingly, ~5% of blastomeres in single cell culture generated extraembryonic yolk syncytial cells, embryonic stem cells and neural crest-derived pigment cells with timings mimicking their appearance in embryos. We revealed the maternal inheritance of key lineage regulators and their differential expression in cleavage embryos. Therefore...

‣ Collective cell guidance by cooperative intercellular forces

Dhananjay T. Tambe; Charles C. Hardin; Jeffrey J. Fredberg; Xavier Trepat
Fonte: Nature Preceedings Publicador: Nature Preceedings
Tipo: Manuscript
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Cells comprising a tissue migrate as part of a collective. In order to coordinate collective multi- cellular migration, each constituent cell integrates local information including chemical signals and mechanical stresses. The boundary between a constituent cell and its immediate neighbors comprises cell-cell junctions and cryptic lamellipodia, but the state of local mechanical stress exerted at that boundary has not been accessible experimentally. As such it is not clear how collective mechanical processes could be coordinated over length scales spanning large multi-cellular assemblies. We report here maps of the stresses exerted within and between cells comprising a monolayer. Within the cell sheet there arise unanticipated fluctuations of mechanical stress that are severe, emerge spontaneously, and ripple across the monolayer. These fluctuations define a rugged stress landscape that becomes increasingly heterogeneous, sluggish, and cooperative with increasing system density. Within that persistently rugged stress landscape, local cellular migrations are found to migrate along local orientations of maximal principal stress. Migrations of both endothelial and epithelial monolayers conform to this behavior, as do breast cancer cell lines before but not after the epithelial-mesenchymal transition. In these diverse cell types...