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  1. Article ; Online: Mammary gland development and EDC-driven cancer susceptibility in mesenchymal ERα-knockout mice.

    Wormsbaecher, Clarissa / Cumbia, Brittney M / Amurgis, Emma G / Poska, Jillian M / Price, Madeline R / Mo, Xiaokui M / Knoblaugh, Sue E / Kurita, Takeshi / Burd, Craig Joseph

    Endocrine-related cancer

    2023  Volume 30, Issue 12

    Abstract: Development of the mammary gland requires both proper hormone signaling and cross talk between the stroma and epithelium. While estrogen receptor (ERα) expression in the epithelium is essential for normal gland development, the role of this receptor in ... ...

    Abstract Development of the mammary gland requires both proper hormone signaling and cross talk between the stroma and epithelium. While estrogen receptor (ERα) expression in the epithelium is essential for normal gland development, the role of this receptor in the stroma is less clear. Moreover, several lines of evidence suggest that mouse phenotypes of in utero exposure to endocrine disruption act through mesenchymal ERα in the developing fetus. We utilized a Twist2-cre mouse line to knock out mesenchymal ERα. Herein, we assessed mammary gland development in the context of mesenchymal ERα deletion. We also tested the effect of in utero bisphenol A (BPA) exposure to alter the tumor susceptibility in the mouse mammary tumor virus-neu (MMTV-neu) breast cancer mouse model. Mesenchymal ERα deletion resulted in altered reproductive tract development and atypical cytology associated with estrous cycling. The mammary gland demonstrated mature epithelial extension unlike complete ERα-knockout mice, but ductal extension was delayed and reduced compared to ERα-competent mice. Using the MMTV-Neu cancer susceptibility model, ERα-intact mice exposed to BPA had reduced tumor-free survival and overall survival compared to BPA-exposed mice having mesenchymal ERα deletion. This difference is specific for BPA exposure as vehicle-treated animals had no difference in tumor development between mice expressing and not expressing mesenchymal ERα. These data demonstrate that mesenchymal ERα expression is not required for ductal extension, nor does it influence cancer risk in this mouse model but does influence the cancer incidence associated with in utero BPA exposure.
    MeSH term(s) Mice ; Animals ; Receptors, Estrogen/metabolism ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Mice, Knockout ; Epithelium/metabolism ; Neoplasms/metabolism ; Mammary Glands, Animal/pathology
    Chemical Substances Receptors, Estrogen ; Estrogen Receptor alpha
    Language English
    Publishing date 2023-11-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1218450-0
    ISSN 1479-6821 ; 1351-0088
    ISSN (online) 1479-6821
    ISSN 1351-0088
    DOI 10.1530/ERC-23-0062
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4192: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  2. Article ; Online: Optimizing extracellular vesicles' isolation from chronic lymphocytic leukemia patient plasma and cell line supernatant.

    Elgamal, Sara / Cocucci, Emanuele / Sass, Ellen J / Mo, Xiaokui M / Blissett, Angela R / Calomeni, Edward P / Rogers, Kerry A / Woyach, Jennifer A / Bhat, Seema A / Muthusamy, Natarajan / Johnson, Amy J / Larkin, Karilyn T / Byrd, John C

    JCI insight

    2021  Volume 6, Issue 15

    Abstract: In chronic lymphocytic leukemia (CLL) and very likely all cancer types, extracellular vesicles (EVs) are a common mechanism by which intercellular messages are communicated between normal, diseased, and transformed cells. Studies of EVs in CLL and other ... ...

    Abstract In chronic lymphocytic leukemia (CLL) and very likely all cancer types, extracellular vesicles (EVs) are a common mechanism by which intercellular messages are communicated between normal, diseased, and transformed cells. Studies of EVs in CLL and other cancers have great variability and often lack reproducibility. For CLL patient plasma and cell lines, we sought to characterize current approaches used in isolating EV products and understand whether cell culture-conditioned media or complex biological fluids confound results. Utilizing nanoparticle tracking analysis, protein quantification, and electron microscopy, we show that ultracentrifugation with an OptiPrep cushion can effectively minimize contaminants from starting materials including plasma and conditioned media of CLL cell lines grown in EV-depleted complete RPMI media but not grown in the serum-free media AIM V commonly used in CLL experimental work. Moreover, we confirm the benefit of including 25 mM trehalose in PBS during EV isolation steps to reduce EV aggregation, to preserve function for downstream applications and characterization. Furthermore, we report the highest particles/μg EVs were obtained from our CLL cell lines utilizing the CELLine bioreactor flask. Finally, we optimized a proliferation assay that offers a functional evaluation of our EVs with minimal sample requirements.
    MeSH term(s) Cell Line ; Chemistry Techniques, Analytical/methods ; Culture Media, Conditioned ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/pathology ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell ; Microscopy, Electron/methods ; Nanoparticles ; Proteins/isolation & purification ; Single Molecule Imaging/instrumentation ; Single Molecule Imaging/methods
    Chemical Substances Culture Media, Conditioned ; Proteins
    Language English
    Publishing date 2021-08-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.137937
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Spinal cord injury causes chronic bone marrow failure.

    Carpenter, Randall S / Marbourg, Jessica M / Brennan, Faith H / Mifflin, Katherine A / Hall, Jodie C E / Jiang, Roselyn R / Mo, Xiaokui M / Karunasiri, Malith / Burke, Matthew H / Dorrance, Adrienne M / Popovich, Phillip G

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 3702

    Abstract: Spinal cord injury (SCI) causes immune dysfunction, increasing the risk of infectious morbidity and mortality. Since bone marrow hematopoiesis is essential for proper immune function, we hypothesize that SCI disrupts bone marrow hematopoiesis. Indeed, ... ...

    Abstract Spinal cord injury (SCI) causes immune dysfunction, increasing the risk of infectious morbidity and mortality. Since bone marrow hematopoiesis is essential for proper immune function, we hypothesize that SCI disrupts bone marrow hematopoiesis. Indeed, SCI causes excessive proliferation of bone marrow hematopoietic stem and progenitor cells (HSPC), but these cells cannot leave the bone marrow, even after challenging the host with a potent inflammatory stimulus. Sequestration of HSPCs in bone marrow after SCI is linked to aberrant chemotactic signaling that can be reversed by post-injury injections of Plerixafor (AMD3100), a small molecule inhibitor of CXCR4. Even though Plerixafor liberates HSPCs and mature immune cells from bone marrow, competitive repopulation assays show that the intrinsic long-term functional capacity of HSPCs is still impaired in SCI mice. Together, our data suggest that SCI causes an acquired bone marrow failure syndrome that may contribute to chronic immune dysfunction.
    MeSH term(s) Animals ; Benzylamines ; Bone Marrow/metabolism ; Bone Marrow/pathology ; Bone Marrow Cells ; Bone Marrow Failure Disorders/etiology ; Bone Marrow Failure Disorders/pathology ; Cell Proliferation ; Chemokine CXCL12 ; Cyclams ; Disease Models, Animal ; Female ; Hematopoiesis ; Hematopoietic Stem Cells/metabolism ; Heterocyclic Compounds/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Transgenic ; Receptors, CXCR4/antagonists & inhibitors ; Signal Transduction ; Spinal Cord Injuries/complications ; Spinal Cord Injuries/immunology
    Chemical Substances Benzylamines ; CXCR4 protein, mouse ; Chemokine CXCL12 ; Cyclams ; Heterocyclic Compounds ; Receptors, CXCR4 ; plerixafor (S915P5499N)
    Language English
    Publishing date 2020-07-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-17564-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: ROR1-targeted delivery of miR-29b induces cell cycle arrest and therapeutic benefit in vivo in a CLL mouse model.

    Chiang, Chi-Ling / Goswami, Swagata / Frissora, Frank W / Xie, Zhiliang / Yan, Pearlly S / Bundschuh, Ralf / Walker, Logan A / Huang, Xiaomeng / Mani, Rajeswaran / Mo, Xiaokui M / Baskar, Sivasubramanian / Rader, Christoph / Phelps, Mitch A / Marcucci, Guido / Byrd, John C / Lee, L James / Muthusamy, Natarajan

    Blood

    2019  Volume 134, Issue 5, Page(s) 432–444

    Abstract: Chronic lymphocytic leukemia (CLL) occurs in 2 major forms: aggressive and indolent. Low miR-29b expression in aggressive CLL is associated with poor prognosis. Indiscriminate miR-29b overexpression in the B-lineage of mice causes aberrance, thus ... ...

    Abstract Chronic lymphocytic leukemia (CLL) occurs in 2 major forms: aggressive and indolent. Low miR-29b expression in aggressive CLL is associated with poor prognosis. Indiscriminate miR-29b overexpression in the B-lineage of mice causes aberrance, thus warranting the need for selective introduction of miR-29b into B-CLL cells for therapeutic benefit. The oncofetal antigen receptor tyrosine kinase orphan receptor 1 (ROR1) is expressed on malignant B-CLL cells, but not normal B cells, encouraging us with ROR1-targeted delivery for therapeutic miRs. Here, we describe targeted delivery of miR-29b to ROR1
    MeSH term(s) Animals ; Biomarkers, Tumor ; Cell Cycle Checkpoints/genetics ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; DNA Methylation ; Disease Models, Animal ; Epigenesis, Genetic ; Humans ; Immunoconjugates/administration & dosage ; Immunoconjugates/chemistry ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/mortality ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Mice ; MicroRNAs/administration & dosage ; MicroRNAs/chemistry ; MicroRNAs/genetics ; Nanoparticles/administration & dosage ; Nanoparticles/chemistry ; Receptor Tyrosine Kinase-like Orphan Receptors/antagonists & inhibitors ; Survival Rate ; Theranostic Nanomedicine ; Treatment Outcome ; Xenograft Model Antitumor Assays
    Chemical Substances Biomarkers, Tumor ; Immunoconjugates ; MIRN29a microRNA, human ; MicroRNAs ; ROR1 protein, human (EC 2.7.10.1) ; Receptor Tyrosine Kinase-like Orphan Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2019-05-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2018882290
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.140: Show issues Location:
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    Zs.MO 364: Show issues

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  5. Article ; Online: IRAK-M promotes alternative macrophage activation and fibroproliferation in bleomycin-induced lung injury.

    Ballinger, Megan N / Newstead, Michael W / Zeng, Xianying / Bhan, Urvashi / Mo, Xiaokui M / Kunkel, Steven L / Moore, Bethany B / Flavell, Richard / Christman, John W / Standiford, Theodore J

    Journal of immunology (Baltimore, Md. : 1950)

    2015  Volume 194, Issue 4, Page(s) 1894–1904

    Abstract: Idiopathic pulmonary fibrosis is a devastating lung disease characterized by inflammation and the development of excessive extracellular matrix deposition. Currently, there are only limited therapeutic intervenes to offer patients diagnosed with ... ...

    Abstract Idiopathic pulmonary fibrosis is a devastating lung disease characterized by inflammation and the development of excessive extracellular matrix deposition. Currently, there are only limited therapeutic intervenes to offer patients diagnosed with pulmonary fibrosis. Although previous studies focused on structural cells in promoting fibrosis, our study assessed the contribution of macrophages. Recently, TLR signaling has been identified as a regulator of pulmonary fibrosis. IL-1R-associated kinase-M (IRAK-M), a MyD88-dependent inhibitor of TLR signaling, suppresses deleterious inflammation, but may paradoxically promote fibrogenesis. Mice deficient in IRAK-M (IRAK-M(-/-)) were protected against bleomycin-induced fibrosis and displayed diminished collagen deposition in association with reduced production of IL-13 compared with wild-type (WT) control mice. Bone marrow chimera experiments indicated that IRAK-M expression by bone marrow-derived cells, rather than structural cells, promoted fibrosis. After bleomycin, WT macrophages displayed an alternatively activated phenotype, whereas IRAK-M(-/-) macrophages displayed higher expression of classically activated macrophage markers. Using an in vitro coculture system, macrophages isolated from in vivo bleomycin-challenged WT, but not IRAK-M(-/-), mice promoted increased collagen and α-smooth muscle actin expression from lung fibroblasts in an IL-13-dependent fashion. Finally, IRAK-M expression is upregulated in peripheral blood cells from idiopathic pulmonary fibrosis patients and correlated with markers of alternative macrophage activation. These data indicate expression of IRAK-M skews lung macrophages toward an alternatively activated profibrotic phenotype, which promotes collagen production, leading to the progression of experimental pulmonary fibrosis.
    MeSH term(s) Animals ; Antibiotics, Antineoplastic/toxicity ; Bleomycin/toxicity ; Blotting, Western ; Cell Separation ; Coculture Techniques ; Collagen ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Female ; Fibroblasts/metabolism ; Humans ; Idiopathic Pulmonary Fibrosis/immunology ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Macrophage Activation/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Real-Time Polymerase Chain Reaction ; Transcriptome
    Chemical Substances Antibiotics, Antineoplastic ; Bleomycin (11056-06-7) ; Collagen (9007-34-5) ; IRAK3 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Irak3 protein, mouse (EC 2.7.11.1)
    Language English
    Publishing date 2015-02-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1402377
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.37: Show issues Location:
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