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  1. Article ; Online: Cellular plasticity: A mechanism for homeostasis in the kidney.

    Assmus, Adrienne M / Mullins, John J / Brown, Cara M / Mullins, Linda J

    Acta physiologica (Oxford, England)

    2020  Volume 229, Issue 1, Page(s) e13447

    Abstract: Cellular plasticity is a topical subject with interest spanning a wide range of fields from developmental biology to regenerative medicine. Even the nomenclature is a subject of debate, and the underlying mechanisms are still under investigation. On top ... ...

    Abstract Cellular plasticity is a topical subject with interest spanning a wide range of fields from developmental biology to regenerative medicine. Even the nomenclature is a subject of debate, and the underlying mechanisms are still under investigation. On top of injury repair, cell plasticity is a constant physiological process in adult organisms and tissues, in response to homeostatic challenges. In this review we discuss two examples of plasticity for the maintenance of homeostasis in the renal system-namely the renin-producing juxtaglomerular cells (JG cells) and cortical collecting duct (CCD) cells. JG cells show plasticity through recruitment mechanisms, answering the demand for an increase in renin production. In the CCD, cells appear to have the ability to transdifferentiate between principal and intercalated cells to help maintain the highly regulated solute transport levels of that segment. These two cases highlight the complexity of plasticity processes and the role they can play in the kidney.
    MeSH term(s) Animals ; Cell Plasticity ; Homeostasis ; Humans ; Kidney/cytology ; Kidney/metabolism ; Renin/metabolism
    Chemical Substances Renin (EC 3.4.23.15)
    Language English
    Publishing date 2020-02-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13447
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Dissociation of sodium-chloride cotransporter expression and blood pressure during chronic high dietary potassium supplementation.

    Little, Robert / Murali, Sathish K / Poulsen, Søren B / Grimm, Paul R / Assmus, Adrienne / Cheng, Lei / Ivy, Jessica R / Hoorn, Ewout J / Matchkov, Vladimir / Welling, Paul A / Fenton, Robert A

    JCI insight

    2023  Volume 8, Issue 5

    Abstract: Dietary potassium (K+) supplementation is associated with a lowering effect in blood pressure (BP), but not all studies agree. Here, we examined the effects of short- and long-term K+ supplementation on BP in mice, whether differences depend on the ... ...

    Abstract Dietary potassium (K+) supplementation is associated with a lowering effect in blood pressure (BP), but not all studies agree. Here, we examined the effects of short- and long-term K+ supplementation on BP in mice, whether differences depend on the accompanying anion or the sodium (Na+) intake and molecular alterations in the kidney that may underlie BP changes. Relative to the control diet, BP was higher in mice fed a high NaCl (1.57% Na+) diet for 7 weeks or fed a K+-free diet for 2 weeks. BP was highest on a K+-free/high NaCl diet. Commensurate with increased abundance and phosphorylation of the thiazide sensitive sodium-chloride-cotransporter (NCC) on the K+-free/high NaCl diet, BP returned to normal with thiazides. Three weeks of a high K+ diet (5% K+) increased BP (predominantly during the night) independently of dietary Na+ or anion intake. Conversely, 4 days of KCl feeding reduced BP. Both feeding periods resulted in lower NCC levels but in increased levels of cleaved (active) α and γ subunits of the epithelial Na+ channel ENaC. The elevated BP after chronic K+ feeding was reduced by amiloride but not thiazide. Our results suggest that dietary K+ has an optimal threshold where it may be most effective for cardiovascular health.
    MeSH term(s) Mice ; Animals ; Blood Pressure ; Sodium Chloride Symporters/metabolism ; Potassium, Dietary ; Sodium Chloride/metabolism ; Epithelial Sodium Channels/metabolism ; Sodium/metabolism ; Thiazides ; Dietary Supplements
    Chemical Substances Sodium Chloride Symporters ; Potassium, Dietary ; Sodium Chloride (451W47IQ8X) ; Epithelial Sodium Channels ; Sodium (9NEZ333N27) ; Thiazides
    Language English
    Publishing date 2023-03-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.156437
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Loss of Adam10 Disrupts Ion Transport in Immortalized Kidney Collecting Duct Cells.

    Assmus, Adrienne / Mullins, Linda / Ward, Mairi / Dobie, Ross / Hunter, Robert / Henderson, Neil C / Mullins, John J

    Function (Oxford, England)

    2021  Volume 2, Issue 4, Page(s) zqab024

    Abstract: The kidney cortical collecting duct (CCD) comprises principal cells (PCs), intercalated cells (IC), and the recently discovered intermediate cell type. Kidney pathology in a mouse model of the syndrome of apparent aldosterone excess revealed plasticity ... ...

    Abstract The kidney cortical collecting duct (CCD) comprises principal cells (PCs), intercalated cells (IC), and the recently discovered intermediate cell type. Kidney pathology in a mouse model of the syndrome of apparent aldosterone excess revealed plasticity of the CCD, with altered PC:intermediate cell:IC ratio. The self-immortalized mouse CCD cell line, mCCD
    MeSH term(s) Animals ; Mice ; ADAM10 Protein/genetics ; Aldosterone/metabolism ; Amyloid Precursor Protein Secretases/genetics ; Cell Line ; Ion Transport/physiology ; Kidney Tubules, Collecting/metabolism ; Membrane Proteins/genetics
    Chemical Substances ADAM10 Protein (EC 3.4.24.81) ; Adam10 protein, mouse (EC 3.4.24.81) ; Aldosterone (4964P6T9RB) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Membrane Proteins
    Language English
    Publishing date 2021-05-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2633-8823
    ISSN (online) 2633-8823
    DOI 10.1093/function/zqab024
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Comparative Studies of Renin-Null Zebrafish and Mice Provide New Functional Insights.

    Hoffmann, Scott / Mullins, Linda / Rider, Sebastien / Brown, Cara / Buckley, Charlotte B / Assmus, Adrienne / Li, Ziwen / Sierra Beltran, Mariana / Henderson, Neil / Del Pozo, Jorge / De Goes Martini, Alexandre / Sequeira-Lopez, Maria Luisa S / Gomez, R Ariel / Mullins, John

    Hypertension (Dallas, Tex. : 1979)

    2022  Volume 79, Issue 3, Page(s) e56–e66

    Abstract: Background: The renin-angiotensin system is highly conserved across vertebrates, including zebrafish, which possess orthologous genes coding for renin-angiotensin system proteins, and specialized mural cells of the kidney arterioles, capable of ... ...

    Abstract Background: The renin-angiotensin system is highly conserved across vertebrates, including zebrafish, which possess orthologous genes coding for renin-angiotensin system proteins, and specialized mural cells of the kidney arterioles, capable of synthesising and secreting renin.
    Methods: We generated zebrafish with CRISPR-Cas9-targeted knockout of renin (
    Results: The
    Conclusions: Phenotypic similarities and transcriptional variations between mouse and zebrafish renin knockouts suggests evolution of renin cell function with terrestrial survival.
    MeSH term(s) Animals ; Animals, Genetically Modified ; Blood Pressure/genetics ; Clustered Regularly Interspaced Short Palindromic Repeats ; Kidney/metabolism ; Mice ; Mice, Knockout ; Renin/genetics ; Renin/metabolism ; Renin-Angiotensin System/physiology ; Transcriptome ; Zebrafish
    Chemical Substances Renin (EC 3.4.23.15)
    Language English
    Publishing date 2022-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.121.18600
    Database MEDical Literature Analysis and Retrieval System OnLINE

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