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  1. Article ; Online: Nitric oxide induces segregation of decay accelerating factor (DAF or CD55) from the membrane lipid-rafts and its internalization in human endometrial cells.

    Banadakoppa, Manu / Goluszko, Pawel / Liebenthal, Daniel / Yallampalli, Chandra

    Cell biology international

    2012  Volume 36, Issue 10, Page(s) 901–907

    Abstract: Recent studies suggest that DAF (decay accelerating factor), a complement regulatory protein, present in lipid rafts, is utilized by Dr fimbriated Escherichia coli for their binding and internalization. Previous studies in our laboratory have shown that ... ...

    Abstract Recent studies suggest that DAF (decay accelerating factor), a complement regulatory protein, present in lipid rafts, is utilized by Dr fimbriated Escherichia coli for their binding and internalization. Previous studies in our laboratory have shown that NO (nitric oxide) can reduce the invasion of Dr(+) E. coli and the severity of uterine infection in pregnant rats. Also, the expression level of DAF both at the mRNA and protein levels has been shown to be reduced by NO. Therefore NO mediated down-regulation of DAF appears to be an important factor in reducing the susceptibility to E. coli infection. However, it is unclear if NO can actually modulate the membrane association of DAF and therefore initial bacterial binding to cells. We found that NO induces the delocalization of DAF from the G(M1)-rich lipid rafts. Using biochemical and cell biological approaches in a uterine epithelial cell model (Ishikawa cells), DAF accumulates in caveolae upon exposure to NO. Interaction of DAF with the caveolar protein, caveolin1, leads to their internalization by endosomes. NO-induced delocalization of DAF from the lipid raft and its accumulation in caveolae are mediated through a cGMP (cyclic guanosine monophosphate) pathway. The acute localized synthesis of NO and its influence on DAF localization may represent an important unrecognized phenomenon of host defence against Dr(+) E. coli bacteria, as well as many disease conditions that involve complement system.
    MeSH term(s) CD55 Antigens/metabolism ; Caveolae/metabolism ; Caveolin 1/metabolism ; Cell Line ; Cyclic GMP/metabolism ; Endometrium/cytology ; Endometrium/microbiology ; Endosomes/metabolism ; Female ; Humans ; Nitric Oxide/metabolism
    Chemical Substances CD55 Antigens ; Caveolin 1 ; Nitric Oxide (31C4KY9ESH) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2012-05-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1143453-3
    ISSN 1095-8355 ; 1065-6995
    ISSN (online) 1095-8355
    ISSN 1065-6995
    DOI 10.1042/CBI20110586
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1451: Show issues Location:
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  2. Article ; Online: Adrenomedullin promotes rat trophoblast stem cell differentiation.

    Gao, Haijun / Liebenthal, Daniel A / Yallampalli, Uma / Yallampalli, Chandra

    Biology of reproduction

    2014  Volume 91, Issue 3, Page(s) 65

    Abstract: Accumulating data suggest that adrenomedullin (ADM) regulates the trophoblast cell growth, migration, and invasion. However, the effect of ADM on trophoblast differentiation is poorly understood. In this study, we hypothesized that ADM promotes the ... ...

    Abstract Accumulating data suggest that adrenomedullin (ADM) regulates the trophoblast cell growth, migration, and invasion. However, the effect of ADM on trophoblast differentiation is poorly understood. In this study, we hypothesized that ADM promotes the differentiation of trophoblast stem cells (TSCs) into trophoblast giant cells (TGCs). Using rat TSCs, Rcho-1 cells, we investigated the effect of ADM on TSC differentiation into TGCs in differentiation or stem cell media, respectively, and explored the effect of ADM on the mechanistic target of rapamycin (MTOR) signaling in trophoblast cell differentiation. The results include: 1) in the presence of differentiation medium, 10⁻⁷ M ADM, but not lower doses, elevated (P < 0.05) Prl3b1/Esrrb (i.e., the ratio of mRNA levels) by 1.7-fold compared to that in control; 2) the supplementation of ADM antagonist, regardless of the concentration of ADM, reduced (P < 0.05) Prl3b1/Esrrb by 2-fold, compared to control group, while the supplementation of CGRP antagonist, regardless of the concentration of ADM, did not change Prl3b1/Esrrb; 3) in the presence of stem cell medium, ADM did not alter the expression of TSC and TGC marker genes, however, the ratio of Prl3b1/Esrrb was reduced (P < 0.05) by ADM antagonist compared to that in control; and 4) ADM increased (P < 0.05) phosphorylated MTOR proteins and the ratio of phosphorylated to total MTOR proteins by 2.0- and 1.7-fold, respectively. The results indicate that ADM promotes but does not induce the differentiation of TSCs to TGCs in a dose-dependent manner and MTOR signaling may play a role in this process.
    MeSH term(s) Adrenomedullin/antagonists & inhibitors ; Adrenomedullin/metabolism ; Adrenomedullin/pharmacology ; Animals ; Antigens, Differentiation/metabolism ; Biomarkers/metabolism ; Calcitonin Gene-Related Peptide/pharmacology ; Calcitonin Receptor-Like Protein/agonists ; Calcitonin Receptor-Like Protein/antagonists & inhibitors ; Calcitonin Receptor-Like Protein/metabolism ; Cell Differentiation/drug effects ; Cell Line ; Cell Size/drug effects ; Gene Expression Regulation/drug effects ; Peptide Fragments/pharmacology ; Phosphorylation/drug effects ; Protein Processing, Post-Translational/drug effects ; Rats ; Receptor Activity-Modifying Protein 2/agonists ; Receptor Activity-Modifying Protein 2/metabolism ; Receptors, Adrenomedullin/agonists ; Receptors, Adrenomedullin/antagonists & inhibitors ; Receptors, Adrenomedullin/metabolism ; Signal Transduction/drug effects ; Stem Cells/cytology ; Stem Cells/drug effects ; Stem Cells/metabolism ; TOR Serine-Threonine Kinases/chemistry ; TOR Serine-Threonine Kinases/metabolism ; Trophoblasts/cytology ; Trophoblasts/drug effects ; Trophoblasts/metabolism
    Chemical Substances Antigens, Differentiation ; Biomarkers ; Calcitonin Receptor-Like Protein ; Calcrl protein, rat ; Peptide Fragments ; Ramp2 protein, rat ; Receptor Activity-Modifying Protein 2 ; Receptors, Adrenomedullin ; adrenomedullin (22-52) ; adrenomedullin receptor, rat ; calcitonin gene-related peptide (8-37) (119911-68-1) ; Adrenomedullin (148498-78-6) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, rat (EC 2.7.1.1) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
    Language English
    Publishing date 2014-07-24
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1118-6
    ISSN 1529-7268 ; 0006-3363
    ISSN (online) 1529-7268
    ISSN 0006-3363
    DOI 10.1095/biolreprod.114.120378
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 551: Show issues Location:
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  3. Article ; Online: PI3K/Akt pathway restricts epithelial adhesion of Dr + Escherichia coli by down-regulating the expression of decay accelerating factor.

    Banadakoppa, Manu / Goluszko, Pawel / Liebenthal, Daniel / Nowicki, Bogdan J / Nowicki, Stella / Yallampalli, Chandra

    Experimental biology and medicine (Maywood, N.J.)

    2014  Volume 239, Issue 5, Page(s) 581–594

    Abstract: The urogenital microbial infection in pregnancy is an important cause of maternal and neonatal morbidity and mortality. Uropathogenic Escherichia coli strains which express Dr fimbriae (Dr+) are associated with unique gestational virulence and they ... ...

    Abstract The urogenital microbial infection in pregnancy is an important cause of maternal and neonatal morbidity and mortality. Uropathogenic Escherichia coli strains which express Dr fimbriae (Dr+) are associated with unique gestational virulence and they utilize cell surface decay accelerating factor (DAF or CD55) as one of the cellular receptor before invading the epithelial cells. Previous studies in our laboratory established that nitric oxide reduces the rate of E. coli invasion by delocalizing the DAF protein from cell surface lipid rafts and down-regulating its expression. The phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) cell signal pathway plays an important role in host-microbe interaction because many bacteria including E. coli activate this pathway in order to establish infection. In the present study, we showed that the PI3K/Akt pathway negatively regulated the expression of DAF on the epithelial cell surface and thus inhibited the adhesion of Dr(+) E. coli to epithelial cells. Initially, using two human cell lines Ishikawa and HeLa which differ in constitutive activity of PI3K/Akt, we showed that DAF levels were associated with the PI3K/Akt pathway. We then showed that the DAF gene expression was up-regulated and the Dr(+) E. coli adhesion increased after the suppression of PI3K/Akt pathway in Ishikawa cells using inhibitor LY294002, and a plasmid which allowed the expression of PI3K/Akt regulatory protein PTEN. The down-regulation of PTEN protein using PTEN-specific siRNA activated the PI3K/Akt pathway, down-regulated the DAF, and decreased the adhesion of Dr(+) E. coli. We conclude that the PI3K/Akt pathway regulated the DAF expression in a nitric oxide independent manner.
    MeSH term(s) 3-Phosphoinositide-Dependent Protein Kinases/metabolism ; Adhesins, Escherichia coli/metabolism ; Bacterial Adhesion ; CD55 Antigens/biosynthesis ; Cell Line ; Down-Regulation ; Enzyme Inhibitors/metabolism ; Epithelial Cells/microbiology ; Epithelial Cells/physiology ; Female ; Gene Knockdown Techniques ; Humans ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Uropathogenic Escherichia coli/physiology
    Chemical Substances Adhesins, Escherichia coli ; CD55 Antigens ; Dr adhesin, E coli ; Enzyme Inhibitors ; 3-Phosphoinositide-Dependent Protein Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2014-03-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 4015-0
    ISSN 1535-3699 ; 1525-1373 ; 0037-9727
    ISSN (online) 1535-3699 ; 1525-1373
    ISSN 0037-9727
    DOI 10.1177/1535370214522183
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ua VI Zs.111: Show issues Location:
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  4. Article ; Online: Role of transcription factor Sp1 and RNA binding protein HuR in the downregulation of Dr+ Escherichia coli receptor protein decay accelerating factor (DAF or CD55) by nitric oxide.

    Banadakoppa, Manu / Liebenthal, Daniel / Nowak, David E / Urvil, Petri / Yallampalli, Uma / Wilson, Gerald M / Kishor, Aparna / Yallampalli, Chandra

    The FEBS journal

    2013  Volume 280, Issue 3, Page(s) 840–854

    Abstract: We previously reported that nitric oxide (NO) reduces the rate of bacteremia and maternal mortality in pregnant rats with uterine infection by Escherichia coli expressing the Dr Fimbria (Dr(+) ). The epithelial invasion of Dr(+) E. coli is dependent on ... ...

    Abstract We previously reported that nitric oxide (NO) reduces the rate of bacteremia and maternal mortality in pregnant rats with uterine infection by Escherichia coli expressing the Dr Fimbria (Dr(+) ). The epithelial invasion of Dr(+) E. coli is dependent on the expression level of its cellular receptor decay accelerating factor (DAF). NO reduces the rate of bacteremia by downregulating the expression of DAF. In this study, we elucidated the role of transcription factor Sp1 and RNA binding protein HuR in the downregulation of human DAF by NO. We generated a series of deletion mutant constructs of DAF gene 5'-untranslated region and mapped the NO-response region upstream to the core promoter region of the DAF gene. One of the several Sp1 binding sites in the DAF 5'-untranslated region was located within the NO-response region. The binding of Sp1 to this site was inhibited by NO. Furthermore, NO also promoted the degradation of DAF mRNA. The 3'-untranslated region of DAF harbors an AU-rich element and this element destabilized the mRNA transcript. NO promoted the rapid degradation of DAF mRNA by inhibiting the binding of mRNA stabilizing protein HuR to this AU-rich region. The inhibition of binding of HuR to the AU-rich region was due to the S-nitrosylation of one or more cysteine residues by NO. Thus, these data reveal the molecular mediators of transcriptional and post-transcriptional regulation of DAF by NO with implications in pathophysiology related to DAF.
    MeSH term(s) 3' Untranslated Regions/genetics ; Binding Sites/genetics ; Blotting, Western ; CD55 Antigens/genetics ; CD55 Antigens/metabolism ; Cell Line, Tumor ; Cysteine/genetics ; Cysteine/metabolism ; Down-Regulation/drug effects ; Down-Regulation/physiology ; ELAV Proteins/genetics ; ELAV Proteins/metabolism ; ELAV Proteins/physiology ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Fimbriae Proteins/genetics ; Fimbriae Proteins/metabolism ; Humans ; Immunoprecipitation ; Mutation ; Nitric Oxide/metabolism ; Nitric Oxide Donors/metabolism ; Nitric Oxide Donors/pharmacology ; Nitroso Compounds/metabolism ; Nitroso Compounds/pharmacology ; Promoter Regions, Genetic/genetics ; Protein Binding ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Regulatory Sequences, Nucleic Acid/genetics ; Sp1 Transcription Factor/genetics ; Sp1 Transcription Factor/metabolism ; Sp1 Transcription Factor/physiology
    Chemical Substances 3' Untranslated Regions ; CD55 Antigens ; ELAV Proteins ; Nitric Oxide Donors ; Nitroso Compounds ; RNA, Messenger ; Sp1 Transcription Factor ; fimbrillin ; 2,2'-(hydroxynitrosohydrazono)bis-ethanamine (146724-94-9) ; Fimbriae Proteins (147680-16-8) ; Nitric Oxide (31C4KY9ESH) ; Cysteine (K848JZ4886)
    Language English
    Publishing date 2013-01-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.12073
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 260: Show issues Location:
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  5. Article: Modulation of 4HNE-mediated signaling by proline-rich peptides from ovine colostrum.

    Boldogh, Istvan / Liebenthal, Daniel / Hughes, T Kley / Juelich, Terry L / Georgiades, Jerzy A / Kruzel, Marian L / Stanton, G John

    Journal of molecular neuroscience : MN

    2003  Volume 20, Issue 2, Page(s) 125–134

    Abstract: In previous studies we showed that colostrinin (CLN), a complex of proline-rich polypeptides derived from ovine colostrum, induces mitogenic stimulation, as well as a variety of cytokines in human peripheral blood leukocytes, and possesses antioxidant ... ...

    Abstract In previous studies we showed that colostrinin (CLN), a complex of proline-rich polypeptides derived from ovine colostrum, induces mitogenic stimulation, as well as a variety of cytokines in human peripheral blood leukocytes, and possesses antioxidant activity in pheochromocytoma (PC12) cells. In this study we investigated the effects of CLN on 4-hydroxynonenal (4HNE)-mediated adduct formation, generation of reactive oxygen species (ROS), glutathione (GSH) metabolism, and the modification of signal transduction cascade that leads to activation of c-Jun N-terminal kinase (JNK) in PC12 cells. Here we demonstrate that CLN (1) reduced the abundance of 4HNE-protein adducts, as shown by fluorescent microscopy and Western blot analysis; (2) reduced intracellular levels of ROS, as shown by a decrease in 2',7'-dichlorodihydro-fluorescein-mediated fluorescence; (3) inhibited 4HNE-mediated GSH depletion, as determined fluorimetrically; and (4) inhibited 4HNE-induced activation of JNKs. Together, these findings suggest that CLN appears to down-regulate 4HNE-mediated lipid peroxidation and its product-induced signaling that otherwise may lead to pathological changes at the cellular and organ level. These findings also suggest further that CLN could be useful in the treatment of diseases such as Alzheimer's, as well as those in which ROS are implicated in pathogenesis.
    MeSH term(s) Aldehydes/antagonists & inhibitors ; Aldehydes/metabolism ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Animals ; Colostrum/metabolism ; Glutathione/metabolism ; JNK Mitogen-Activated Protein Kinases ; Lipid Peroxidation/drug effects ; Lipid Peroxidation/physiology ; Mitogen-Activated Protein Kinases/drug effects ; Mitogen-Activated Protein Kinases/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Peptides/pharmacology ; Peptides/therapeutic use ; Rats ; Reactive Oxygen Species/antagonists & inhibitors ; Reactive Oxygen Species/metabolism ; Sheep ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Tumor Suppressor Protein p53/drug effects ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Aldehydes ; Peptides ; Reactive Oxygen Species ; Tumor Suppressor Protein p53 ; colostrinine ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Glutathione (GAN16C9B8O) ; 4-hydroxy-2-nonenal (K1CVM13F96)
    Language English
    Publishing date 2003-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1043392-2
    ISSN 0895-8696
    ISSN 0895-8696
    DOI 10.1385/JMN:20:2:125
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3006: Show issues Location:
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