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  1. Article ; Online: Retinoic acid signaling in mouse retina endothelial cells is required for early angiogenic growth.

    Como, Christina N / Cervantes, Cesar / Pawlikowski, Brad / Siegenthaler, Julie

    Differentiation; research in biological diversity

    2022  Volume 130, Page(s) 16–27

    Abstract: The development of the retinal vasculature is essential to maintain health of the tissue, but the developmental mechanisms are not completely understood. The aim of this study was to investigate the cell-autonomous role of retinoic acid signaling in ... ...

    Abstract The development of the retinal vasculature is essential to maintain health of the tissue, but the developmental mechanisms are not completely understood. The aim of this study was to investigate the cell-autonomous role of retinoic acid signaling in endothelial cells during retina vascular development. Using a temporal and cell-specific mouse model to disrupt retinoic acid signaling in endothelial cells in the postnatal retina (Pdgfb
    MeSH term(s) Mice ; Animals ; Endothelial Cells/metabolism ; Tretinoin ; Retina ; Signal Transduction ; Retinal Vessels/metabolism
    Chemical Substances Tretinoin (5688UTC01R)
    Language English
    Publishing date 2022-12-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 184540-8
    ISSN 1432-0436 ; 0301-4681
    ISSN (online) 1432-0436
    ISSN 0301-4681
    DOI 10.1016/j.diff.2022.12.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1170: Show issues Location:
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  2. Article ; Online: Retinoic acid signaling in vascular development.

    Pawlikowski, Brad / Wragge, Jacob / Siegenthaler, Julie A

    Genesis (New York, N.Y. : 2000)

    2019  Volume 57, Issue 7-8, Page(s) e23287

    Abstract: Formation of the vasculature is an essential developmental process, delivering oxygen and nutrients to support cellular processes needed for tissue growth and maturation. Retinoic acid (RA) and its downstream signaling pathway is vital for normal pre- ... ...

    Abstract Formation of the vasculature is an essential developmental process, delivering oxygen and nutrients to support cellular processes needed for tissue growth and maturation. Retinoic acid (RA) and its downstream signaling pathway is vital for normal pre- and post-natal development, playing key roles in the specification and formation of many organs and tissues. Here, we review the role of RA in blood and lymph vascular development, beginning with embryonic yolk sac vasculogenesis and remodeling and discussing RA's organ-specific roles in angiogenesis and vessel maturation. In particular, we highlight the multi-faceted role of RA signaling in CNS vascular development and acquisition of blood-brain barrier properties.
    MeSH term(s) Animals ; Blood Vessels/embryology ; Blood Vessels/metabolism ; Humans ; Lymphatic Vessels/embryology ; Lymphatic Vessels/metabolism ; Neovascularization, Physiologic ; Signal Transduction ; Tretinoin/metabolism
    Chemical Substances Tretinoin (5688UTC01R)
    Language English
    Publishing date 2019-03-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2004544-X
    ISSN 1526-968X ; 1526-954X
    ISSN (online) 1526-968X
    ISSN 1526-954X
    DOI 10.1002/dvg.23287
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2772: Show issues Location:
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  3. Article ; Online: Aging disrupts gene expression timing during muscle regeneration.

    Kurland, Jesse V / Cutler, Alicia A / Stanley, Jacob T / Betta, Nicole Dalla / Van Deusen, Ashleigh / Pawlikowski, Brad / Hall, Monica / Antwine, Tiffany / Russell, Alan / Allen, Mary Ann / Dowell, Robin / Olwin, Bradley

    Stem cell reports

    2023  Volume 18, Issue 6, Page(s) 1325–1339

    Abstract: Skeletal muscle function and regenerative capacity decline during aging, yet factors driving these changes are incompletely understood. Muscle regeneration requires temporally coordinated transcriptional programs to drive myogenic stem cells to activate, ...

    Abstract Skeletal muscle function and regenerative capacity decline during aging, yet factors driving these changes are incompletely understood. Muscle regeneration requires temporally coordinated transcriptional programs to drive myogenic stem cells to activate, proliferate, fuse to form myofibers, and to mature as myonuclei, restoring muscle function after injury. We assessed global changes in myogenic transcription programs distinguishing muscle regeneration in aged mice from young mice by comparing pseudotime trajectories from single-nucleus RNA sequencing of myogenic nuclei. Aging-specific differences in coordinating myogenic transcription programs necessary for restoring muscle function occur following muscle injury, likely contributing to compromised regeneration in aged mice. Differences in pseudotime alignment of myogenic nuclei when comparing aged with young mice via dynamic time warping revealed pseudotemporal differences becoming progressively more severe as regeneration proceeds. Disruptions in timing of myogenic gene expression programs may contribute to incomplete skeletal muscle regeneration and declines in muscle function as organisms age.
    MeSH term(s) Animals ; Mice ; Cell Nucleus ; Stem Cells ; Aging/genetics ; Muscle, Skeletal ; Gene Expression
    Language English
    Publishing date 2023-06-12
    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.2023.05.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Formation and function of the meningeal arachnoid barrier around the developing mouse brain.

    Derk, Julia / Como, Christina N / Jones, Hannah E / Joyce, Luke R / Kim, Sol / Spencer, Brady L / Bonney, Stephanie / O'Rourke, Rebecca / Pawlikowski, Brad / Doran, Kelly S / Siegenthaler, Julie A

    Developmental cell

    2023  Volume 58, Issue 8, Page(s) 635–644.e4

    Abstract: The arachnoid barrier, a component of the blood-cerebrospinal fluid barrier (B-CSFB) in the meninges, is composed of epithelial-like, tight-junction-expressing cells. Unlike other central nervous system (CNS) barriers, its' developmental mechanisms and ... ...

    Abstract The arachnoid barrier, a component of the blood-cerebrospinal fluid barrier (B-CSFB) in the meninges, is composed of epithelial-like, tight-junction-expressing cells. Unlike other central nervous system (CNS) barriers, its' developmental mechanisms and timing are largely unknown. Here, we show that mouse arachnoid barrier cell specification requires the repression of Wnt-β-catenin signaling and that constitutively active β-catenin can prevent its formation. We also show that the arachnoid barrier is functional prenatally and, in its absence, a small molecular weight tracer and the bacterium group B Streptococcus can cross into the CNS following peripheral injection. Acquisition of barrier properties prenatally coincides with the junctional localization of Claudin 11, and increased E-cadherin and maturation continues after birth, where postnatal expansion is marked by proliferation and re-organization of junctional domains. This work identifies fundamental mechanisms that drive arachnoid barrier formation, highlights arachnoid barrier fetal functions, and provides novel tools for future studies on CNS barrier development.
    MeSH term(s) Mice ; Animals ; beta Catenin ; Meninges ; Arachnoid ; Blood-Brain Barrier ; Central Nervous System ; Tight Junctions
    Chemical Substances beta Catenin
    Language English
    Publishing date 2023-03-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2023.03.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5742: Show issues Location:
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    Zs.MG 76: Show issues

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  5. Article: Mirk/dyrk1B is a Rho-induced kinase active in skeletal muscle differentiation.

    Deng, Xiaobing / Ewton, Daina Z / Pawlikowski, Brad / Maimone, Margaret / Friedman, Eileen

    The Journal of biological chemistry

    2003  Volume 278, Issue 42, Page(s) 41347–41354

    Abstract: The Rho family of small GTPases regulates numerous signaling pathways that control the organization of the cytoskeleton, transcription factor activity, and many aspects of the differentiation of skeletal myoblasts. We now demonstrate that the kinase Mirk ...

    Abstract The Rho family of small GTPases regulates numerous signaling pathways that control the organization of the cytoskeleton, transcription factor activity, and many aspects of the differentiation of skeletal myoblasts. We now demonstrate that the kinase Mirk (minibrain-related kinase)/dyrk1B is induced by members of the Rho-family in myoblasts and that Mirk is active in skeletal muscle differentiation. Mirk is an arginine-directed serine/threonine kinase which is expressed at elevated levels in skeletal muscle compared with other normal tissues. A Mirk promoter construct was activated when C2C12 myoblasts were switched from growth to differentiation medium and was also activated by the Rho family members RhoA, Cdc42, and to a lesser degree Rac1, but not by MyoD or Myf5. Mirk protein levels increased following transient expression of constitutively active Cdc42-QL, RhoA-QL, or Rac1-QL in C2C12 cells. High concentrations of serum mitogens down-regulated Mirk through activation of the Ras-MEK-Erk pathway. As a result, Mirk transcription was induced by the MEK1 inhibitor PD98059 and by the switch from growth to differentiation medium. Mirk was induced with similar kinetics to another Rho-induced differentiation gene, myogenin. Mirk protein levels increased 10-fold within 24-48 h after primary cultured muscle cells; C2C12 mouse myoblasts or L6 rat myoblasts were induced to differentiate. Thus Mirk was induced following the commitment stage of myogenesis. Stable overexpression of Mirk enabled myoblasts to fuse more rapidly when placed in differentiation medium. The function of Mirk in muscle differentiation was established by depletion of endogenous Mirk by small interfering RNA, which prevented myoblast fusion into myotubes and inhibited induction of markers of differentiation, including myogenin, fast twitch troponin T, and muscle myosin heavy chain. Other members of the dyrk/minibrain/HIPK family of kinases in lower organisms have been shown to regulate the transition from growth to differentiation, and Mirk is now shown to participate in skeletal muscle development.
    MeSH term(s) Animals ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Gene Deletion ; Kinetics ; Mice ; Muscle, Skeletal/cytology ; Muscle, Skeletal/metabolism ; Muscles/metabolism ; Myogenin/metabolism ; Plasmids/metabolism ; Promoter Regions, Genetic ; Protein Serine-Threonine Kinases/metabolism ; Protein Serine-Threonine Kinases/physiology ; Protein-Tyrosine Kinases/metabolism ; Protein-Tyrosine Kinases/physiology ; RNA Interference ; RNA, Messenger/metabolism ; Rats ; Time Factors ; Tissue Distribution ; Transfection ; Dyrk Kinases
    Chemical Substances Enzyme Inhibitors ; Myog protein, mouse ; Myog protein, rat ; Myogenin ; RNA, Messenger ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2003-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M306780200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.108: Show issues Location:
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