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  1. Article ; Online: Mouse Ex Vivo Kidney Culture Methods.

    Ihermann-Hella, Anneliis / Kuure, Satu

    Methods in molecular biology (Clifton, N.J.)

    2019  Volume 1926, Page(s) 23–30

    Abstract: Kidney organogenesis has been a widely used classical model system to study inductive tissue interactions that guide differentiation of many organs. The basis for this is in the pioneering work done during the early 1950s when the conditions of how to ... ...

    Abstract Kidney organogenesis has been a widely used classical model system to study inductive tissue interactions that guide differentiation of many organs. The basis for this is in the pioneering work done during the early 1950s when the conditions of how to support ex vivo growth and differentiation of developing kidneys were revealed. Importantly, culturing developing kidneys remains as an essential instrument to advance our understanding of molecular and cellular regulation of morphogenesis even today. Despite the fact that embryonic kidneys have been cultured for decades, it is not a trivial method and requires specific anatomical and developmental biology knowledge. This chapter outlines the general steps in organ culture and details the requirements for successful kidney explant differentiation.
    MeSH term(s) Animals ; Cell Differentiation ; Kidney/cytology ; Kidney/embryology ; Mesoderm/cytology ; Mice ; Organ Culture Techniques/methods ; Ureter/cytology ; Ureter/enzymology
    Language English
    Publishing date 2019-02-11
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-9021-4_2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: FGF8 induces chemokinesis and regulates condensation of mouse nephron progenitor cells.

    Sharma, Abhishek / Meer, Marco / Dapkunas, Arvydas / Ihermann-Hella, Anneliis / Kuure, Satu / Vainio, Seppo J / Iber, Dagmar / Naillat, Florence

    Development (Cambridge, England)

    2022  Volume 149, Issue 21

    Abstract: Kidneys develop via iterative branching of the ureteric epithelial tree and subsequent nephrogenesis at the branch points. Nephrons form in the cap mesenchyme as the metanephric mesenchyme (MM) condenses around the epithelial ureteric buds (UBs). ... ...

    Abstract Kidneys develop via iterative branching of the ureteric epithelial tree and subsequent nephrogenesis at the branch points. Nephrons form in the cap mesenchyme as the metanephric mesenchyme (MM) condenses around the epithelial ureteric buds (UBs). Previous work has demonstrated that FGF8 is important for the survival of nephron progenitor cells (NPCs), and early deletion of Fgf8 leads to the cessation of nephron formation, which results in post-natal lethality. We now reveal a previously unreported function of FGF8. By combining transgenic mouse models, quantitative imaging assays and data-driven computational modelling, we show that FGF8 has a strong chemokinetic effect and that this chemokinetic effect is important for the condensation of NPCs to the UB. The computational model shows that the motility must be lower close to the UB to achieve NPC attachment. We conclude that the FGF8 signalling pathway is crucial for the coordination of NPC condensation at the UB. Chemokinetic effects have also been described for other FGFs and may be generally important for the formation of mesenchymal condensates.
    MeSH term(s) Mice ; Animals ; Nephrons/metabolism ; Kidney/metabolism ; Organogenesis ; Fibroblast Growth Factors/metabolism ; Stem Cells/metabolism ; Mice, Transgenic ; Fibroblast Growth Factor 8/genetics ; Fibroblast Growth Factor 8/metabolism
    Chemical Substances Fibroblast Growth Factors (62031-54-3) ; Fgf8 protein, mouse ; Fibroblast Growth Factor 8 (148997-75-5)
    Language English
    Publishing date 2022-10-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.201012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 91: Show issues

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  3. Article ; Online: Comparative whole-genome transcriptome analysis in renal cell populations reveals high tissue specificity of MAPK/ERK targets in embryonic kidney.

    Kurtzeborn, Kristen / Kwon, Hyuk Nam / Iaroshenko, Vladislav / Faisal, Imrul / Ambrož, Martin / Jin, Xing / Qureshi, Talha / Kupari, Jussi / Ihermann-Hella, Anneliis / Väänänen, Juho / Tyynismaa, Henna / Boušová, Iva / Park, Sunghyouk / Kuure, Satu

    BMC biology

    2022  Volume 20, Issue 1, Page(s) 112

    Abstract: Background: MAPK/ERK signaling is a well-known mediator of extracellular stimuli controlling intracellular responses to growth factors and mechanical cues. The critical requirement of MAPK/ERK signaling for embryonic stem cell maintenance is ... ...

    Abstract Background: MAPK/ERK signaling is a well-known mediator of extracellular stimuli controlling intracellular responses to growth factors and mechanical cues. The critical requirement of MAPK/ERK signaling for embryonic stem cell maintenance is demonstrated, but specific functions in progenitor regulation during embryonic development, and in particular kidney development remain largely unexplored. We previously demonstrated MAPK/ERK signaling as a key regulator of kidney growth through branching morphogenesis and normal nephrogenesis where it also regulates progenitor expansion. Here, we performed RNA sequencing-based whole-genome expression analysis to identify transcriptional MAPK/ERK targets in two distinct renal populations: the ureteric bud epithelium and the nephron progenitors.
    Results: Our analysis revealed a large number (5053) of differentially expressed genes (DEGs) in nephron progenitors and significantly less (1004) in ureteric bud epithelium, reflecting likely heterogenicity of cell types. The data analysis identified high tissue-specificity, as only a fraction (362) of MAPK/ERK targets are shared between the two tissues. Tissue-specific MAPK/ERK targets participate in the regulation of mitochondrial energy metabolism in nephron progenitors, which fail to maintain normal mitochondria numbers in the MAPK/ERK-deficient tissue. In the ureteric bud epithelium, a dramatic decline in progenitor-specific gene expression was detected with a simultaneous increase in differentiation-associated genes, which was not observed in nephron progenitors. Our experiments in the genetic model of MAPK/ERK deficiency provide evidence that MAPK/ERK signaling in the ureteric bud maintains epithelial cells in an undifferentiated state. Interestingly, the transcriptional targets shared between the two tissues studied are over-represented by histone genes, suggesting that MAPK/ERK signaling regulates cell cycle progression and stem cell maintenance through chromosome condensation and nucleosome assembly.
    Conclusions: Using tissue-specific MAPK/ERK inactivation and RNA sequencing in combination with experimentation in embryonic kidneys, we demonstrate here that MAPK/ERK signaling maintains ureteric bud tip cells, suggesting a regulatory role in collecting duct progenitors. We additionally deliver new mechanistic information on how MAPK/ERK signaling regulates progenitor maintenance through its effects on chromatin accessibility and energy metabolism.
    MeSH term(s) Epithelial Cells ; Female ; Gene Expression Profiling ; Humans ; Kidney/metabolism ; Nephrons/metabolism ; Organ Specificity ; Pregnancy
    Language English
    Publishing date 2022-05-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2133020-7
    ISSN 1741-7007 ; 1741-7007
    ISSN (online) 1741-7007
    ISSN 1741-7007
    DOI 10.1186/s12915-022-01309-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Dynamic MAPK/ERK Activity Sustains Nephron Progenitors through Niche Regulation and Primes Precursors for Differentiation.

    Ihermann-Hella, Anneliis / Hirashima, Tsuyoshi / Kupari, Jussi / Kurtzeborn, Kristen / Li, Hao / Kwon, Hyuk Nam / Cebrian, Cristina / Soofi, Abdul / Dapkunas, Arvydas / Miinalainen, Ilkka / Dressler, Gregory R / Matsuda, Michiyuki / Kuure, Satu

    Stem cell reports

    2018  Volume 11, Issue 4, Page(s) 912–928

    Abstract: The in vivo niche and basic cellular properties of nephron progenitors are poorly described. Here we studied the cellular organization and function of the MAPK/ERK pathway in nephron progenitors. Live-imaging of ERK activity by a Förster resonance energy ...

    Abstract The in vivo niche and basic cellular properties of nephron progenitors are poorly described. Here we studied the cellular organization and function of the MAPK/ERK pathway in nephron progenitors. Live-imaging of ERK activity by a Förster resonance energy transfer biosensor revealed a dynamic activation pattern in progenitors, whereas differentiating precursors exhibited sustained activity. Genetic experiments demonstrate that MAPK/ERK activity controls the thickness, coherence, and integrity of the nephron progenitor niche. Molecularly, MAPK/ERK activity regulates niche organization and communication with extracellular matrix through PAX2 and ITGA8, and is needed for CITED1 expression denoting undifferentiated status. MAPK/ERK activation in nephron precursors propels differentiation by priming cells for distal and proximal fates induced by the Wnt and Notch pathways. Thus, our results demonstrate a mechanism through which MAPK/ERK activity controls both progenitor maintenance and differentiation by regulating a distinct set of targets, which maintain the biomechanical milieu of tissue-residing progenitors and prime precursors for nephrogenesis.
    MeSH term(s) Animals ; Apoptosis ; Biosensing Techniques ; Body Patterning ; Cell Differentiation ; Cell Proliferation ; Cell Self Renewal ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression Regulation, Developmental ; Integrin alpha Chains/metabolism ; Mice ; Nephrons/cytology ; Organogenesis ; PAX2 Transcription Factor/metabolism ; Stem Cell Niche ; Stem Cells/cytology ; Stem Cells/metabolism
    Chemical Substances Integrin alpha Chains ; PAX2 Transcription Factor ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2018-09-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2720528-9
    ISSN 2213-6711 ; 2213-6711
    ISSN (online) 2213-6711
    ISSN 2213-6711
    DOI 10.1016/j.stemcr.2018.08.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Mitogen-activated protein kinase (MAPK) pathway regulates branching by remodeling epithelial cell adhesion.

    Ihermann-Hella, Anneliis / Lume, Maria / Miinalainen, Ilkka J / Pirttiniemi, Anniina / Gui, Yujuan / Peränen, Johan / Charron, Jean / Saarma, Mart / Costantini, Frank / Kuure, Satu

    PLoS genetics

    2014  Volume 10, Issue 3, Page(s) e1004193

    Abstract: Although the growth factor (GF) signaling guiding renal branching is well characterized, the intracellular cascades mediating GF functions are poorly understood. We studied mitogen-activated protein kinase (MAPK) pathway specifically in the branching ... ...

    Abstract Although the growth factor (GF) signaling guiding renal branching is well characterized, the intracellular cascades mediating GF functions are poorly understood. We studied mitogen-activated protein kinase (MAPK) pathway specifically in the branching epithelia of developing kidney by genetically abrogating the pathway activity in mice lacking simultaneously dual-specificity protein kinases Mek1 and Mek2. Our data show that MAPK pathway is heterogeneously activated in the subset of G1- and S-phase epithelial cells, and its tissue-specific deletion results in severe renal hypodysplasia. Consequently to the deletion of Mek1/2, the activation of ERK1/2 in the epithelium is lost and normal branching pattern in mutant kidneys is substituted with elongation-only phenotype, in which the epithelium is largely unable to form novel branches and complex three-dimensional patterns, but able to grow without primary defects in mitosis. Cellular characterization of double mutant epithelium showed increased E-cadherin at the cell surfaces with its particular accumulation at baso-lateral locations. This indicates changes in cellular adhesion, which were revealed by electron microscopic analysis demonstrating intercellular gaps and increased extracellular space in double mutant epithelium. When challenged to form monolayer cultures, the mutant epithelial cells were impaired in spreading and displayed strong focal adhesions in addition to spiky E-cadherin. Inhibition of MAPK activity reduced paxillin phosphorylation on serine 83 while remnants of phospho-paxillin, together with another focal adhesion (FA) protein vinculin, were augmented at cell surface contacts. We show that MAPK activity is required for branching morphogenesis, and propose that it promotes cell cycle progression and higher cellular motility through remodeling of cellular adhesions.
    MeSH term(s) Animals ; Epithelial Cells/metabolism ; Focal Adhesions/genetics ; Kidney/growth & development ; Kidney/metabolism ; MAP Kinase Kinase 1/genetics ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 2/genetics ; MAP Kinase Kinase 2/metabolism ; MAP Kinase Signaling System/genetics ; Mice ; Mitogen-Activated Protein Kinases/genetics ; Morphogenesis/genetics ; Phosphorylation ; Signal Transduction/genetics ; Vinculin/metabolism
    Chemical Substances Vinculin (125361-02-6) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2) ; Map2k1 protein, mouse (EC 2.7.12.2) ; Map2k2 protein, mouse (EC 2.7.12.2)
    Language English
    Publishing date 2014-03-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1004193
    Database MEDical Literature Analysis and Retrieval System OnLINE

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