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  1. Article ; Online: Putting the pressure on endocytosis in the kidney.

    Van Giel, Dorien / Vennekens, Rudi

    Cell calcium

    2020  Volume 94, Page(s) 102338

    Abstract: In Science Signaling, Gualdani and colleagues provide evidence that the ion channel TRPV4 functions as a mechanosensor in the renal proximal tubules and show that TRPV4 activity modulates protein reabsorption. ...

    Abstract In Science Signaling, Gualdani and colleagues provide evidence that the ion channel TRPV4 functions as a mechanosensor in the renal proximal tubules and show that TRPV4 activity modulates protein reabsorption.
    MeSH term(s) Albumins ; Endocytosis ; Kidney Tubules, Proximal ; TRPV Cation Channels
    Chemical Substances Albumins ; TRPV Cation Channels
    Language English
    Publishing date 2020-12-26
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2020.102338
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1596: 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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  2. Article ; Online: The adaptive roles of aneuploidy and polyclonality in Leishmania in response to environmental stress.

    Negreira, Gabriel H / de Groote, Robin / Van Giel, Dorien / Monsieurs, Pieter / Maes, Ilse / de Muylder, Geraldine / Van den Broeck, Frederik / Dujardin, Jean-Claude / Domagalska, Malgorzata A

    EMBO reports

    2023  Volume 24, Issue 9, Page(s) e57413

    Abstract: Aneuploidy is generally considered harmful, but in some microorganisms, it can act as an adaptive mechanism against environmental stress. Here, we use Leishmania-a protozoan parasite with remarkable genome plasticity-to study the early steps of ... ...

    Abstract Aneuploidy is generally considered harmful, but in some microorganisms, it can act as an adaptive mechanism against environmental stress. Here, we use Leishmania-a protozoan parasite with remarkable genome plasticity-to study the early steps of aneuploidy evolution under high drug pressure (using antimony or miltefosine as stressors). By combining single-cell genomics, lineage tracing with cellular barcodes, and longitudinal genome characterization, we reveal that aneuploidy changes under antimony pressure result from polyclonal selection of pre-existing karyotypes, complemented by further and rapid de novo alterations in chromosome copy number along evolution. In the case of miltefosine, early parasite adaptation is associated with independent point mutations in a miltefosine transporter gene, while aneuploidy changes only emerge later, upon exposure to increased drug levels. Therefore, polyclonality and genome plasticity are hallmarks of parasite adaptation, but the scenario of aneuploidy dynamics depends on the nature and strength of the environmental stress as well as on the existence of other pre-adaptive mechanisms.
    MeSH term(s) Humans ; Leishmania/genetics ; Antimony ; Chromosomes ; Aneuploidy
    Chemical Substances Antimony (9IT35J3UV3) ; miltefosine (53EY29W7EC)
    Language English
    Publishing date 2023-07-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.202357413
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5433: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 41: Show issues

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  3. Article ; Online: Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death.

    Decuypere, Jean-Paul / Van Giel, Dorien / Janssens, Peter / Dong, Ke / Somlo, Stefan / Cai, Yiqiang / Mekahli, Djalila / Vennekens, Rudi

    International journal of molecular sciences

    2021  Volume 22, Issue 24

    Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is mainly caused by deficiency of polycystin-1 (PC1) or polycystin-2 (PC2). Altered autophagy has recently been implicated in ADPKD progression, but its exact regulation by PC1 and PC2 remains unclear. ...

    Abstract Autosomal dominant polycystic kidney disease (ADPKD) is mainly caused by deficiency of polycystin-1 (PC1) or polycystin-2 (PC2). Altered autophagy has recently been implicated in ADPKD progression, but its exact regulation by PC1 and PC2 remains unclear. We therefore investigated cell death and survival during nutritional stress in mouse inner medullary collecting duct cells (mIMCDs), either wild-type (WT) or lacking PC1 (PC1KO) or PC2 (PC2KO), and human urine-derived proximal tubular epithelial cells (PTEC) from early-stage ADPKD patients with PC1 mutations versus healthy individuals. Basal autophagy was enhanced in PC1-deficient cells. Similarly, following starvation, autophagy was enhanced and cell death reduced when PC1 was reduced. Autophagy inhibition reduced cell death resistance in PC1KO mIMCDs to the WT level, implying that PC1 promotes autophagic cell survival. Although PC2 expression was increased in PC1KO mIMCDs, PC2 knockdown did not result in reduced autophagy. PC2KO mIMCDs displayed lower basal autophagy, but more autophagy and less cell death following chronic starvation. This could be reversed by overexpression of PC1 in PC2KO. Together, these findings indicate that PC1 levels are partially coupled to PC2 expression, and determine the transition from renal cell survival to death, leading to enhanced survival of ADPKD cells during nutritional stress.
    MeSH term(s) Animals ; Autophagy/physiology ; Cell Death/physiology ; Cell Line ; Epithelial Cells/metabolism ; Humans ; Kidney Tubules, Proximal/metabolism ; Mice ; Polycystic Kidney, Autosomal Dominant/metabolism ; Starvation/metabolism ; TRPP Cation Channels/metabolism
    Chemical Substances TRPP Cation Channels
    Language English
    Publishing date 2021-12-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222413511
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Enhanced MCP-1 Release in Early Autosomal Dominant Polycystic Kidney Disease.

    Janssens, Peter / Decuypere, Jean-Paul / De Rechter, Stéphanie / Breysem, Luc / Van Giel, Dorien / Billen, Jaak / Hindryckx, An / De Catte, Luc / Baldewijns, Marcella / Claes, Kathleen B M / Wissing, Karl M / Devriendt, Koen / Bammens, Bert / Meyts, Isabelle / Torres, Vicente E / Vennekens, Rudi / Mekahli, Djalila

    Kidney international reports

    2021  Volume 6, Issue 6, Page(s) 1687–1698

    Abstract: Introduction: Autosomal dominant polycystic kidney disease (ADPKD) causes kidney failure typically in adulthood, but the disease starts : Methods: In a cross-sectional study, plasma copeptin, urinary EGF, and urinary MCP-1 were evaluated in a ... ...

    Abstract Introduction: Autosomal dominant polycystic kidney disease (ADPKD) causes kidney failure typically in adulthood, but the disease starts
    Methods: In a cross-sectional study, plasma copeptin, urinary EGF, and urinary MCP-1 were evaluated in a pediatric ADPKD cohort and compared with age-, sex-, and body mass index (BMI)-matched healthy controls. MCP-1 was studied in mouse collecting duct cells, human proximal tubular cells, and fetal kidney tissue.
    Results: Fifty-three genotyped ADPKD patients and 53 controls were included. The mean (SD) age was 10.4 (5.9) versus 10.5 (6.1) years (
    Conclusion: An increase in tubular MCP-1 secretion is an early event in ADPKD. MCP-1 is an early disease severity marker and a potential treatment target.
    Language English
    Publishing date 2021-04-06
    Publishing country United States
    Document type Journal Article
    ISSN 2468-0249
    ISSN (online) 2468-0249
    DOI 10.1016/j.ekir.2021.03.893
    Database MEDical Literature Analysis and Retrieval System OnLINE

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