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  1. Article ; Online: Reindeer light the way to scarless wound healing.

    Caves, Elizabeth / Horsley, Valerie

    Cell

    2022  Volume 185, Issue 25, Page(s) 4675–4677

    Abstract: Wound healing in adult mammalian tissues generally involves scarring instead of tissue regeneration. A study in this issue of Cell reveals that after injury, reindeer antler skin regenerates by priming regenerative genes in wound fibroblasts instead of ... ...

    Abstract Wound healing in adult mammalian tissues generally involves scarring instead of tissue regeneration. A study in this issue of Cell reveals that after injury, reindeer antler skin regenerates by priming regenerative genes in wound fibroblasts instead of forming a scar through an inflammatory gene program.
    Language English
    Publishing date 2022-12-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2022.11.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1167: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 58: Show issues

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  2. Article ; Online: IL-6 trans-signaling in a humanized mouse model of scleroderma.

    Odell, Ian D / Agrawal, Kriti / Sefik, Esen / Odell, Anahi V / Caves, Elizabeth / Kirkiles-Smith, Nancy C / Horsley, Valerie / Hinchcliff, Monique / Pober, Jordan S / Kluger, Yuval / Flavell, Richard A

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Volume 120, Issue 37, Page(s) e2306965120

    Abstract: Fibrosis is regulated by interactions between immune and mesenchymal cells. However, the capacity of cell types to modulate human fibrosis pathology is poorly understood due to lack of a fully humanized model system. MISTRG6 mice were engineered by ... ...

    Abstract Fibrosis is regulated by interactions between immune and mesenchymal cells. However, the capacity of cell types to modulate human fibrosis pathology is poorly understood due to lack of a fully humanized model system. MISTRG6 mice were engineered by homologous mouse/human gene replacement to develop an immune system like humans when engrafted with human hematopoietic stem cells (HSCs). We utilized MISTRG6 mice to model scleroderma by transplantation of healthy or scleroderma skin from a patient with pansclerotic morphea to humanized mice engrafted with unmatched allogeneic HSC. We identified that scleroderma skin grafts contained both skin and bone marrow-derived human CD4 and CD8 T cells along with human endothelial cells and pericytes. Unlike healthy skin, fibroblasts in scleroderma skin were depleted and replaced by mouse fibroblasts. Furthermore, HSC engraftment alleviated multiple signatures of fibrosis, including expression of collagen and interferon genes, and proliferation and activation of human T cells. Fibrosis improvement correlated with reduced markers of T cell activation and expression of human IL-6 by mesenchymal cells. Mechanistic studies supported a model whereby IL-6 trans-signaling driven by CD4 T cell-derived soluble IL-6 receptor complexed with fibroblast-derived IL-6 promoted excess extracellular matrix gene expression. Thus, MISTRG6 mice transplanted with scleroderma skin demonstrated multiple fibrotic responses centered around human IL-6 signaling, which was improved by the presence of healthy bone marrow-derived immune cells. Our results highlight the importance of IL-6 trans-signaling in pathogenesis of scleroderma and the ability of healthy bone marrow-derived immune cells to mitigate disease.
    MeSH term(s) Humans ; Animals ; Mice ; Scleroderma, Localized ; Interleukin-6 ; Endothelial Cells ; Skin ; Disease Models, Animal ; Basidiomycota
    Chemical Substances Interleukin-6
    Language English
    Publishing date 2023-09-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2306965120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Erratum for Caves et al., "Air-Liquid Interface Method To Study Epstein-Barr Virus Pathogenesis in Nasopharyngeal Epithelial Cells".

    Caves, Elizabeth A / Cook, Sarah A / Lee, Nara / Stoltz, Donna / Watkins, Simon / Shair, Kathy H Y

    mSphere

    2019  Volume 4, Issue 2

    Language English
    Publishing date 2019-04-17
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ISSN 2379-5042
    ISSN (online) 2379-5042
    DOI 10.1128/mSphere.00247-19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Air-Liquid Interface Method To Study Epstein-Barr Virus Pathogenesis in Nasopharyngeal Epithelial Cells.

    Caves, Elizabeth A / Cook, Sarah A / Lee, Nara / Stoltz, Donna / Watkins, Simon / Shair, Kathy H Y

    mSphere

    2018  Volume 3, Issue 4

    Abstract: Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that establishes a latent reservoir in peripheral B-lymphocytes with sporadic reactivation. EBV also infects epithelial cells, predominantly resulting in a lytic infection, which may contribute to ...

    Abstract Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that establishes a latent reservoir in peripheral B-lymphocytes with sporadic reactivation. EBV also infects epithelial cells, predominantly resulting in a lytic infection, which may contribute to EBV transmission from saliva. In the nasopharynx, EBV infection can lead to the clonal expansion of a latently infected cell and the development of nasopharyngeal carcinoma (NPC). The mechanisms governing EBV pathogenesis in nasopharyngeal epithelium are largely unknown. An advanced understanding would depend on a physiologically relevant culture model of polarized airway epithelium. The recent application of the organotypic raft culture in keratinocytes has demonstrated great promise for the use of polarized cultures in the study of EBV permissive replication. In this study, the adaptation of an air-liquid interface (ALI) culture method using transwell membranes was explored in an EBV-infected NPC cell line. In the EBV-infected NPC HK1 cell line, ALI culture resulted in the completion of EBV reactivation, with global induction of the lytic cascade, replication of EBV genomes, and production of infectious progeny virus. We propose that the ALI culture method can be widely adopted as a physiologically relevant model to study EBV pathogenesis in polarized nasal epithelial cells.
    Importance: Lifting adherent cells to the air-liquid interface (ALI) is a method conventionally used to culture airway epithelial cells into polarized apical and basolateral surfaces. Reactivation of Epstein-Barr virus (EBV) from monolayer epithelial cultures is sometimes abortive, which may be attributed to the lack of authentic reactivation triggers that occur in stratified epithelium
    MeSH term(s) Cell Line ; Epithelial Cells/virology ; Herpesvirus 4, Human/pathogenicity ; Herpesvirus 4, Human/physiology ; Host-Pathogen Interactions ; Humans ; Models, Biological ; Nasopharynx/virology ; Virus Activation ; Virus Cultivation/methods ; Virus Replication
    Keywords covid19
    Language English
    Publishing date 2018-07-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-5042
    ISSN (online) 2379-5042
    DOI 10.1128/mSphere.00152-18
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Skin Fibrosis and Recovery Is Dependent on Wnt Activation via DPP4.

    Jussila, Anna R / Zhang, Brian / Caves, Elizabeth / Kirti, Sakin / Steele, Miarasa / Hamburg-Shields, Emily / Lydon, John / Ying, Yan / Lafyatis, Robert / Rajagopalan, Sanjay / Horsley, Valerie / Atit, Radhika P

    The Journal of investigative dermatology

    2021  Volume 142, Issue 6, Page(s) 1597–1606.e9

    Abstract: Fibrosis is the life-threatening, excessive accumulation of the extracellular matrix and is sometimes associated with a loss of lipid-filled cells in the skin and other organs. Understanding the mechanisms of fibrosis and associated lipodystrophy and ... ...

    Abstract Fibrosis is the life-threatening, excessive accumulation of the extracellular matrix and is sometimes associated with a loss of lipid-filled cells in the skin and other organs. Understanding the mechanisms of fibrosis and associated lipodystrophy and their reversal may reveal new targets for therapeutic intervention. In vivo genetic models are needed to identify key targets that induce recovery from established fibrosis. Wnt signaling is activated in animal and human fibrotic diseases across organs. Here, we developed a genetically inducible and reversible Wnt activation model and showed that it is sufficient to cause fibrotic dermal remodeling, including extracellular matrix expansion and shrinking of dermal adipocytes. Upon withdrawal from Wnt activation, Wnt-induced fibrotic remodeling was reversed in mouse skin-fully restoring skin architecture. Next, we demonstrated CD26/ DPP4 is a Wnt/β-catenin-responsive gene and a functional mediator of fibrotic transformation. We provide genetic evidence that the Wnt/DPP4 axis is required to drive fibrotic dermal remodeling and is associated with human skin fibrosis severity. Remarkably, DPP4 inhibitors can be repurposed to accelerate recovery from established Wnt-induced fibrosis. Collectively, this study identifies Wnt/DPP4 axis as a key driver of extracellular matrix homeostasis and dermal fat loss, providing therapeutic avenues to manipulate the onset and reversal of tissue fibrosis.
    MeSH term(s) Animals ; Dipeptidyl Peptidase 4/genetics ; Fibroblasts/metabolism ; Fibrosis ; Mice ; Skin/pathology ; Skin Diseases/genetics ; Skin Diseases/pathology ; Wnt Signaling Pathway ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances beta Catenin ; Dipeptidyl Peptidase 4 (EC 3.4.14.5) ; Dpp4 protein, mouse (EC 3.4.14.5)
    Language English
    Publishing date 2021-11-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2021.10.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui VI Zs.124: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  6. Article: Latent Membrane Protein 1 Is a Novel Determinant of Epstein-Barr Virus Genome Persistence and Reactivation.

    Caves, Elizabeth A / Butch, Rachel M / Cook, Sarah A / Wasil, Laura R / Chen, Chen / Di, Yuanpu Peter / Lee, Nara / Shair, Kathy H Y

    mSphere

    2017  Volume 2, Issue 6

    Abstract: Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that persistently infects humans, with nearly 95% seropositivity in adults. Infection in differentiating epithelia is permissive, but EBV-associated nasopharyngeal carcinoma (NPC) tumors harbor a ... ...

    Abstract Epstein-Barr virus (EBV) is a ubiquitous gammaherpesvirus that persistently infects humans, with nearly 95% seropositivity in adults. Infection in differentiating epithelia is permissive, but EBV-associated nasopharyngeal carcinoma (NPC) tumors harbor a clonal and nonproductive latent infection. However, in explanted NPC cultures and epithelial cell lines, episomal EBV genomes are frequently lost. The resulting unstable infection has hampered efforts to study the determinants of EBV persistence and latency in epithelial oncogenesis. The EBV nuclear antigen 1 (EBNA1) protein is required for tethering EBV episomes to cellular DNA and for mitotic segregation to daughter cells. Expression of EBNA1 does not ensure faithful partitioning of EBV episomes or replicons, suggesting that additional regulatory mechanisms have yet to be elucidated. The EBV latent membrane protein 1 (LMP1) is an oncogenic signaling protein expressed in latent and lytic cycles. This study identified that LMP1 contributes to the loss of EBV genomes in latently infected cells and promotes differentiation-induced lytic replication in a polarized air-liquid interface (ALI) culture model. Deletion of LMP1 in recombinantly infected 293 cells promoted the retention of EBV genomes in passaged cells, which was in part localized to a conserved PXQXT motif in the C-terminal signaling domain (CTAR1). Additionally, knockdown of LMP1 in the recombinantly infected NPC cell line HK1 resulted in decreased induction of lytic proteins and infectious EBV titers. These findings are consistent with the hypothesis that in epithelial infections, regulation of LMP1 mechanisms may be a determinant of infection outcome and a potential risk factor for EBV persistence in preneoplastic cells.
    Language English
    Publishing date 2017-11-08
    Publishing country United States
    Document type Journal Article
    ISSN 2379-5042
    ISSN 2379-5042
    DOI 10.1128/mSphereDirect.00453-17
    Database MEDical Literature Analysis and Retrieval System OnLINE

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