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  1. AU="Cirio, Maria Cecilia"
  2. AU="Rodriguez-Rodriguez, Alvaro Manuel"
  3. AU="Anna Maria Aloisi"
  4. AU="Na, Li"
  5. AU="Beatriz Aguiar Jordão Paranhos"
  6. AU="johnson, Michael"
  7. AU=Hunt S A
  8. AU="Gniazdowski, Victoria"
  9. AU="Griffin, Matthew E"
  10. AU="Bean, Paris"
  11. AU="Elomaa, Paula"
  12. AU="Robert Fowler"
  13. AU="Nielsen, Stine"
  14. AU="Chabartier, Cyrille"

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  1. Artikel: Zebrafish Models of Kidney Damage and Repair.

    Cirio, Maria Cecilia / de Caestecker, Mark P / Hukriede, Neil A

    Current pathobiology reports

    2015  Band 3, Heft 2, Seite(n) 163–170

    Abstract: The vertebrate kidney possesses the capacity to repair damaged nephrons, and this potential is conserved regardless of the complexity of species-specific kidneys. However, many aquatic vertebrates possess the ability to not only repair existing nephrons, ...

    Abstract The vertebrate kidney possesses the capacity to repair damaged nephrons, and this potential is conserved regardless of the complexity of species-specific kidneys. However, many aquatic vertebrates possess the ability to not only repair existing nephrons, but also generate new nephrons after injury. Adult zebrafish have the ability to recover from acute renal injury not only by replacing lost injured epithelial cells of endogenous nephrons, but by also generating de novo nephrons. This strong regeneration potential, along with other unique characteristics such as the high degree of genetic conservation with humans, the ease of harvesting externally fertilized, transparent embryos, the accessibility to larval and adult kidneys, and the ability to perform whole organism phenotypic small molecule screens, has positioned zebrafish as a unique vertebrate model to study kidney injury. In this review, we provide an overview of the contribution of zebrafish larvae/adult studies to the understanding of renal regeneration, diseases, and therapeutic discovery.
    Sprache Englisch
    Erscheinungsdatum 2015-04-11
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2167-485X
    ISSN 2167-485X
    DOI 10.1007/s40139-015-0080-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Development of high-content assays for kidney progenitor cell expansion in transgenic zebrafish.

    Sanker, Subramaniam / Cirio, Maria Cecilia / Vollmer, Laura L / Goldberg, Natasha D / McDermott, Lee A / Hukriede, Neil A / Vogt, Andreas

    Journal of biomolecular screening

    2013  Band 18, Heft 10, Seite(n) 1193–1202

    Abstract: Reactivation of genes normally expressed during organogenesis is a characteristic of kidney regeneration. Enhancing this reactivation could potentially be a therapeutic target to augment kidney regeneration. The inductive events that drive kidney ... ...

    Abstract Reactivation of genes normally expressed during organogenesis is a characteristic of kidney regeneration. Enhancing this reactivation could potentially be a therapeutic target to augment kidney regeneration. The inductive events that drive kidney organogenesis in zebrafish are similar to the initial steps in mammalian kidney organogenesis. Therefore, quantifying embryonic signals that drive zebrafish kidney development is an attractive strategy for the discovery of potential novel therapeutic modalities that accelerate kidney regeneration. The Lim1 homeobox protein, Lhx1, is a marker of kidney development that is also expressed in the regenerating kidneys after injury. Using a fluorescent Lhx1a-EGFP transgene whose phenotype faithfully recapitulates that of the endogenous protein, we developed a high-content assay for Lhx1a-EGFP expression in transgenic zebrafish embryos employing an artificial intelligence-based image analysis method termed cognition network technology (CNT). Implementation of the CNT assay on high-content readers enabled automated real-time in vivo time-course, dose-response, and variability studies in the developing embryo. The Lhx1a assay was complemented with a kidney-specific secondary CNT assay that enables direct measurements of the embryonic renal tubule cell population. The integration of fluorescent transgenic zebrafish embryos with automated imaging and artificial intelligence-based image analysis provides an in vivo analysis system for structure-activity relationship studies and de novo discovery of novel agents that augment innate regenerative processes.
    Mesh-Begriff(e) Animals ; Biological Assay ; Cell Proliferation/drug effects ; Drug Evaluation, Preclinical/methods ; Embryo, Nonmammalian/drug effects ; Embryo, Nonmammalian/metabolism ; Gene Expression/drug effects ; Green Fluorescent Proteins/biosynthesis ; Green Fluorescent Proteins/genetics ; Histone Deacetylase Inhibitors/pharmacology ; Kidney/cytology ; Kidney/physiology ; LIM-Homeodomain Proteins/genetics ; LIM-Homeodomain Proteins/metabolism ; Phenylbutyrates/pharmacology ; Recombinant Fusion Proteins/biosynthesis ; Recombinant Fusion Proteins/genetics ; Regeneration ; Stem Cells/drug effects ; Stem Cells/physiology ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Zebrafish ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemische Substanzen Histone Deacetylase Inhibitors ; LIM-Homeodomain Proteins ; Lhx1a protein, zebrafish ; Phenylbutyrates ; Recombinant Fusion Proteins ; Transcription Factors ; Zebrafish Proteins ; enhanced green fluorescent protein ; methyl-4-(phenylthio)butanoate ; Green Fluorescent Proteins (147336-22-9)
    Sprache Englisch
    Erscheinungsdatum 2013-07-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1433680-7
    ISSN 1552-454X ; 1087-0571
    ISSN (online) 1552-454X
    ISSN 1087-0571
    DOI 10.1177/1087057113495296
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Leukemia inhibitory factor induces apoptosis of the mammary epithelial cells and participates in mouse mammary gland involution.

    Schere-Levy, Carolina / Buggiano, Valeria / Quaglino, Ana / Gattelli, Albana / Cirio, Maria Cecilia / Piazzon, Isabel / Vanzulli, Silvia / Kordon, Edith C

    Experimental cell research

    2003  Band 282, Heft 1, Seite(n) 35–47

    Abstract: Leukemia inhibitory factor (LIF) is a multifunctional glycoprotein that displays multiple biological activities in different cell types, but to date there has been no report on its expression in the normal mammary gland. In this study we found that LIF ... ...

    Abstract Leukemia inhibitory factor (LIF) is a multifunctional glycoprotein that displays multiple biological activities in different cell types, but to date there has been no report on its expression in the normal mammary gland. In this study we found that LIF is expressed at low but detectable levels in postpubertal, adult virgin, and pregnant mouse mammary glands. However, LIF expression drops after parturition to become almost undetectable in lactating glands. Interestingly, LIF expression shows a steep increase shortly after weaning that is maintained for the following 3 days. During this period, known as the first stage of mammary gland involution, the lack of suckling induces local factors that cause extensive epithelial cell death. It has been shown that Stat3 is the main factor in signaling the initiation of apoptosis, but the mechanism of its activation remains unclear. Herein, we show that LIF expression in the gland is induced by milk stasis and not by the decrease of circulating lactogenic hormones after weaning. Implantation of LIF containing pellets in lactating glands results in a significant increase in epithelium apoptosis. In addition, this treatment also induces Stat3 phosphorylation. We conclude that LIF regulated expression in the mouse mammary gland may play a relevant role during the first stage of mammary gland involution. Our results also show that LIF-induced mammary epithelium apoptosis could be mediated, at least partially, by Stat3 activation.
    Mesh-Begriff(e) Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; DNA-Binding Proteins/metabolism ; Epithelial Cells/cytology ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Estrous Cycle/physiology ; Female ; Glucocorticoids/metabolism ; Glucocorticoids/pharmacology ; Growth Inhibitors/genetics ; Growth Inhibitors/metabolism ; Growth Inhibitors/pharmacology ; Interleukin-6 ; Lactation/drug effects ; Lactation/physiology ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/genetics ; Lymphokines/metabolism ; Lymphokines/pharmacology ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/drug effects ; Mammary Glands, Animal/metabolism ; Mice ; Mice, Inbred BALB C ; RNA, Messenger/drug effects ; RNA, Messenger/metabolism ; Receptors, Cytokine/genetics ; Receptors, OSM-LIF ; STAT3 Transcription Factor ; Trans-Activators/metabolism
    Chemische Substanzen DNA-Binding Proteins ; Glucocorticoids ; Growth Inhibitors ; Interleukin-6 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lif protein, mouse ; Lifr protein, mouse ; Lymphokines ; RNA, Messenger ; Receptors, Cytokine ; Receptors, OSM-LIF ; STAT3 Transcription Factor ; Stat3 protein, mouse ; Trans-Activators
    Sprache Englisch
    Erscheinungsdatum 2003-01-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1006/excr.2002.5666
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Progression of pregnancy-dependent mouse mammary tumors after long dormancy periods. Involvement of Wnt pathway activation.

    Gattelli, Albana / Cirio, María Cecilia / Quaglino, Ana / Schere-Levy, Carolina / Martinez, Natalia / Binaghi, María / Meiss, Roberto P / Castilla, Lucio H / Kordon, Edith C

    Cancer research

    2004  Band 64, Heft 15, Seite(n) 5193–5199

    Abstract: Mouse mammary tumor virus (LA) induces pregnancy-dependent mammary tumors that progress toward autonomy. Here we show that in virgin females, pregnancy-dependent tumor transplants are able to remain dormant for up to 300 days. During that period, these ... ...

    Abstract Mouse mammary tumor virus (LA) induces pregnancy-dependent mammary tumors that progress toward autonomy. Here we show that in virgin females, pregnancy-dependent tumor transplants are able to remain dormant for up to 300 days. During that period, these tumors synthesize DNA, express high levels of estrogen and progesterone receptors (ER+PR+) and are able to resume growth after hormone stimulation. Surprisingly, in a subsequent transplant generation, all these tumors are fully able to grow in virgin females, they express low levels of ER and PR (ER-PR-) and have a monoclonal origin; i.e., show all of the features we have described previously in pregnancy-independent tumors. Histologically, mouse mammary tumor virus (LA)-induced tumors are morphologically similar to genetically engineered mouse (GEM) mammary tumors that overexpress genes belonging to the Wnt pathway. Interestingly, in the virus-induced neoplasias, pregnancy-independent passages arising after a dormant phase usually display a lower level of glandular differentiation together with epithelial cell trans-differentiation, a specific feature associated to Wnt pathway activation. In addition, dormancy can lead to the specific selection of Int2/Fgf3 mutated and overexpressing cells. Therefore, our results indicate that during hormone-dependent tumor dormancy, relevant changes in cell population occur, allowing rapid progression after changes in the animal internal milieu.
    Mesh-Begriff(e) Animals ; Apoptosis ; Base Sequence ; Cell Differentiation ; Cell Division ; Disease Progression ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Female ; Fibroblast Growth Factor 3 ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mammary Neoplasms, Experimental/virology ; Mammary Tumor Virus, Mouse/pathogenicity ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; Neoplasm Transplantation ; Neoplasms, Hormone-Dependent ; Pregnancy ; Pregnancy Complications, Neoplastic/metabolism ; Proto-Oncogene Proteins/metabolism ; Receptors, Estrogen/metabolism ; Receptors, Progesterone/metabolism ; Signal Transduction ; Time Factors ; Wnt2 Protein
    Chemische Substanzen Fgf3 protein, mouse ; Fibroblast Growth Factor 3 ; Proto-Oncogene Proteins ; Receptors, Estrogen ; Receptors, Progesterone ; Wnt2 Protein ; Fibroblast Growth Factors (62031-54-3)
    Sprache Englisch
    Erscheinungsdatum 2004-08-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-03-3992
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Origin and progression of pregnancy-dependent mammary tumors induced by new mouse mammary tumor virus variants.

    Buggiano, Valeria / Levy, Carolina Schere / Gattelli, Albana / Cirio, María Cecilia / Marfil, Mariana / Nepomnaschy, Irene / Piazzon, Isabel / Helguero, Luisa / Vanzulli, Silvia / Kordon, Edith C

    Breast cancer research and treatment

    2002  Band 75, Heft 3, Seite(n) 191–202

    Abstract: In order to study mechanisms of progression of mouse mammary tumor virus (MMTV)-induced pregnancy-dependent mammary lesions, we removed and serially transplanted 17 small tumors detected in MMTV-infected pregnant females. This gave rise to the same ... ...

    Abstract In order to study mechanisms of progression of mouse mammary tumor virus (MMTV)-induced pregnancy-dependent mammary lesions, we removed and serially transplanted 17 small tumors detected in MMTV-infected pregnant females. This gave rise to the same number of 'in vivo' tumor lines. Hormone-dependency of the passages was determined by comparing tumor development in multiparous versus virgin hosts. We found that the first passages of most of these lesions (11/17) required pregnancy to grow. However, all these tumor lines lost their hormone-dependence through successive passages. The original pregnancy-dependent lesions were mostly multiclonal and showed high levels of estrogen and progesterone receptors. Alternatively, pregnancy-independent tumors arose as clonal dominant populations exhibiting a lower hormone receptor content. Our data show that the progression of hormone-dependent MMTV-induced mammary tumors is an irreversible process associated with the appearance of additional MMTV insertional events as well as alterations in the composition of the tumor cell population.
    Mesh-Begriff(e) Animals ; DNA, Neoplasm/metabolism ; Disease Progression ; Estrogens/metabolism ; Female ; Mammary Neoplasms, Experimental/metabolism ; Mammary Neoplasms, Experimental/pathology ; Mammary Neoplasms, Experimental/virology ; Mammary Tumor Virus, Mouse/pathogenicity ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Neoplasms, Hormone-Dependent/metabolism ; Neoplasms, Hormone-Dependent/pathology ; Neoplasms, Hormone-Dependent/virology ; Pregnancy ; Pregnancy, Animal ; Progesterone/metabolism ; Receptors, Estrogen/metabolism ; Receptors, Progesterone/metabolism
    Chemische Substanzen DNA, Neoplasm ; Estrogens ; Receptors, Estrogen ; Receptors, Progesterone ; Progesterone (4G7DS2Q64Y)
    Sprache Englisch
    Erscheinungsdatum 2002-02-28
    Erscheinungsland Netherlands
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604563-7
    ISSN 1573-7217 ; 0167-6806
    ISSN (online) 1573-7217
    ISSN 0167-6806
    DOI 10.1023/a:1019932516887
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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