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  1. Article ; Online: Collapsing Focal Segmental Glomerulosclerosis in Viral Infections.

    Muehlig, Anne K / Gies, Sydney / Huber, Tobias B / Braun, Fabian

    Frontiers in immunology

    2022  Volume 12, Page(s) 800074

    Abstract: Collapsing glomerulopathy represents a special variant of the proteinuric kidney disease focal segmental glomerulosclerosis (FSGS). Histologically, the collapsing form of FSGS (cFSGS) is characterized by segmental or global condensation and obliteration ... ...

    Abstract Collapsing glomerulopathy represents a special variant of the proteinuric kidney disease focal segmental glomerulosclerosis (FSGS). Histologically, the collapsing form of FSGS (cFSGS) is characterized by segmental or global condensation and obliteration of glomerular capillaries, the appearance of hyperplastic and hypertrophic podocytes and severe tubulointerstitial damage. Clinically, cFSGS patients present with acute kidney injury, nephrotic-range proteinuria and are at a high risk of rapid progression to irreversible kidney failure. cFSGS can be attributed to numerous etiologies, namely, viral infections like HIV, cytomegalovirus, Epstein-Barr-Virus, and parvovirus B19 and also drugs and severe ischemia. Risk variants of the APOL1 gene, predominantly found in people of African descent, increase the risk of developing cFSGS. Patients infected with the new Corona-Virus SARS-CoV-2 display an increased rate of acute kidney injury (AKI) in severe cases of COVID-19. Besides hemodynamic instability, cytokine mediated injury and direct viral entry and infection of renal epithelial cells contributing to AKI, there are emerging reports of cFSGS associated with SARS-CoV-2 infection in patients of mainly African ethnicity. The pathogenesis of cFSGS is proposed to be linked with direct viral infection of podocytes, as described for HIV-associated glomerulopathy. Nevertheless, there is growing evidence that the systemic inflammatory cascade, activated in acute viral infections like COVID-19, is a major contributor to the impairment of basic cellular functions in podocytes. This mini review will summarize the current knowledge on cFSGS associated with viral infections with a special focus on the influence of systemic immune responses and potential mechanisms propagating the development of cFSGS.
    MeSH term(s) Animals ; COVID-19/complications ; COVID-19/immunology ; COVID-19/virology ; Epithelial Cells/immunology ; Epithelial Cells/virology ; Glomerulosclerosis, Focal Segmental/etiology ; Glomerulosclerosis, Focal Segmental/immunology ; Glomerulosclerosis, Focal Segmental/virology ; Humans ; Immunity/immunology ; Kidney Glomerulus/immunology ; Kidney Glomerulus/virology ; Podocytes/immunology ; Podocytes/virology ; Proteinuria/etiology ; Proteinuria/immunology ; Proteinuria/virology ; SARS-CoV-2/immunology
    Language English
    Publishing date 2022-01-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.800074
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Online ; Thesis: Der Einfluss von Hypoxie und HIF-1U+03B1 auf die Interaktion von humanen CD4+25- und CD4+25high T-Zellen sowie die Entwicklung von T-Helfer-Zellen Typ 17

    Gies, Sydney Elisabeth [Verfasser]

    2016  

    Author's details Sydney Elisabeth Gies
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Zentrale Hochschulbibliothek Lübeck
    Publishing place Lübeck
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  3. Article ; Online: Ibrutinib-associated focal segmental glomerulosclerosis and the impact of podocin mutations in chronic lymphocytic leukemia.

    Czogalla, Jan / Schliffke, Simon / Lu, Shun / Schwerk, Maria / Petereit, Helena / Zhang, Tianran / Liu, Shuya / Dumoulin, Bernhard / Gies, Sydney / Wu, Guochao / Hänzelmann, Sonja / Bode, Marlies / Grahammer, Florian / Gödel, Markus / Voigtländer, Minna / Butt, Linus / Bokemeyer, Carsten / Bergmann, Carsten / Benzing, Thomas /
    Wiech, Thorsten / Puelles, Victor G / Huber, Tobias B

    Kidney international

    2024  Volume 105, Issue 4, Page(s) 877–881

    MeSH term(s) Humans ; Glomerulosclerosis, Focal Segmental/chemically induced ; Glomerulosclerosis, Focal Segmental/drug therapy ; Glomerulosclerosis, Focal Segmental/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Mutation ; Nephrotic Syndrome/genetics ; Adenine/analogs & derivatives ; Membrane Proteins ; Piperidines ; Intracellular Signaling Peptides and Proteins
    Chemical Substances NPHS2 protein ; ibrutinib (1X70OSD4VX) ; Adenine (JAC85A2161) ; Membrane Proteins ; Piperidines ; Intracellular Signaling Peptides and Proteins
    Language English
    Publishing date 2024-02-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2024.02.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 797: 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)
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  4. Article ; Online: Single-cell transcriptomics reveals a mechanosensitive injury signaling pathway in early diabetic nephropathy.

    Liu, Shuya / Zhao, Yu / Lu, Shun / Zhang, Tianran / Lindenmeyer, Maja T / Nair, Viji / Gies, Sydney E / Wu, Guochao / Nelson, Robert G / Czogalla, Jan / Aypek, Hande / Zielinski, Stephanie / Liao, Zhouning / Schaper, Melanie / Fermin, Damian / Cohen, Clemens D / Delic, Denis / Krebs, Christian F / Grahammer, Florian /
    Wiech, Thorsten / Kretzler, Matthias / Meyer-Schwesinger, Catherine / Bonn, Stefan / Huber, Tobias B

    Genome medicine

    2023  Volume 15, Issue 1, Page(s) 2

    Abstract: Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and histopathologic glomerular lesions are among the earliest structural alterations of DN. However, the signaling pathways that initiate these glomerular alterations ...

    Abstract Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and histopathologic glomerular lesions are among the earliest structural alterations of DN. However, the signaling pathways that initiate these glomerular alterations are incompletely understood.
    Methods: To delineate the cellular and molecular basis for DN initiation, we performed single-cell and bulk RNA sequencing of renal cells from type 2 diabetes mice (BTBR ob/ob) at the early stage of DN.
    Results: Analysis of differentially expressed genes revealed glucose-independent responses in glomerular cell types. The gene regulatory network upstream of glomerular cell programs suggested the activation of mechanosensitive transcriptional pathway MRTF-SRF predominantly taking place in mesangial cells. Importantly, activation of MRTF-SRF transcriptional pathway was also identified in DN glomeruli in independent patient cohort datasets. Furthermore, ex vivo kidney perfusion suggested that the regulation of MRTF-SRF is a common mechanism in response to glomerular hyperfiltration.
    Conclusions: Overall, our study presents a comprehensive single-cell transcriptomic landscape of early DN, highlighting mechanosensitive signaling pathways as novel targets of diabetic glomerulopathy.
    MeSH term(s) Mice ; Animals ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Transcriptome ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Signal Transduction
    Language English
    Publishing date 2023-01-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
    ZDB-ID 2484394-5
    ISSN 1756-994X ; 1756-994X
    ISSN (online) 1756-994X
    ISSN 1756-994X
    DOI 10.1186/s13073-022-01145-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Transcription regulates HIF-1α expression in CD4(+) T cells.

    Bollinger, Thomas / Bollinger, Annalena / Gies, Sydney / Feldhoff, Lea / Solbach, Werner / Rupp, Jan

    Immunology and cell biology

    2015  Volume 94, Issue 1, Page(s) 109–113

    Abstract: The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4(+) T cells (T cells) remains elusive. Here we observed that depletion of oxygen ( ...

    Abstract The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4(+) T cells (T cells) remains elusive. Here we observed that depletion of oxygen (O2⩽2%) alone was not sufficient to induce HIF-1α expression in T cells. However, when hypoxic T cells were stimulated, HIF-1α was expressed and this was dependent on nuclear factor-κB- and nuclear factor of activated T cell (NFAT)-mediated transcriptional upregulation of Hif-1α mRNA. HIF-1α upregulation could be blocked by drugs inhibiting NF-κB, NFAT or mammalian target of rapamycin precluding CD4(+) T-cell stimulation or translation in T cells, as well as by blocking transcription. CD3, CD28, phorbol-12-myristat-13-acetat (PMA) or ionomycin-stimulated T cells did not express HIF-1α under normoxic conditions. In conclusion, regulation of HIF-1α expression in CD4(+) T cells in hypoxia gravely relies on its transcriptional upregulation and subsequent enhanced protein stabilization.
    MeSH term(s) CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Female ; Gene Expression Regulation ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Lymphocyte Activation/immunology ; Male ; Protein Stability ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic
    Chemical Substances Hypoxia-Inducible Factor 1, alpha Subunit ; RNA, Messenger
    Language English
    Publishing date 2015-07-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 284057-1
    ISSN 1440-1711 ; 0818-9641
    ISSN (online) 1440-1711
    ISSN 0818-9641
    DOI 10.1038/icb.2015.64
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.175: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  6. Article ; Online: HIF-1α- and hypoxia-dependent immune responses in human CD4+CD25high T cells and T helper 17 cells.

    Bollinger, Thomas / Gies, Sydney / Naujoks, Julius / Feldhoff, Lea / Bollinger, Annalena / Solbach, Werner / Rupp, Jan

    Journal of leukocyte biology

    2014  Volume 96, Issue 2, Page(s) 305–312

    Abstract: The central oxygen sensitive transcription factor HIF-1α has been implicated in the differentiation of n(T(reg)) and Th17 cells and to orchestrate metabolic changes of activated T cells. However, data on the functional relevance of HIF-1α and Hox, in ... ...

    Abstract The central oxygen sensitive transcription factor HIF-1α has been implicated in the differentiation of n(T(reg)) and Th17 cells and to orchestrate metabolic changes of activated T cells. However, data on the functional relevance of HIF-1α and Hox, in general, for nT(reg)-suppressive activity and T cell function in primary human cells are still missing. Therefore, we analyzed the effect of Hox and HIF-1α on human T(res), n(Treg), and Th17 cells. Under Hox, nT(reg)-mediated suppression of T(res) proliferation, CD25 expression, and secretion of IFN-γ were significantly reduced, whereas expression levels of VEGF, TNF-α, and IL-10 were significantly increased. In contrast to observations in mice, Th17 lineage commitment, as determined by RORγt expression, was not affected by activation or inhibition of HIF-1α expression using DMOG or YC-1 treatment, respectively. Nevertheless, the secretion of IL-17A was increased by DMOG and reduced by YC-1 under Th17-skewing conditions in a dose- dependent manner. In conclusion, Hox and HIF-1α substantially influence human T cell-mediated immune responses by modulation of nT(reg)-suppressive function and IL-17A secretion by Th17 cells.
    MeSH term(s) Animals ; CD4 Antigens/immunology ; Cytokines/immunology ; Enzyme Activators/pharmacology ; Female ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/immunology ; Indazoles/pharmacology ; Interleukin-2 Receptor alpha Subunit/immunology ; Male ; Mice ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/cytology ; Th17 Cells/immunology
    Chemical Substances CD4 Antigens ; Cytokines ; Enzyme Activators ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; IL2RA protein, human ; Indazoles ; Interleukin-2 Receptor alpha Subunit ; 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (154453-18-6)
    Language English
    Publishing date 2014-08
    Publishing country United States
    Document type Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.3A0813-426RR
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: 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)
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