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  1. Article ; Online: PIEZO1 regulates leader cell formation and cellular coordination during collective keratinocyte migration.

    Chen, Jinghao / Holt, Jesse R / Evans, Elizabeth L / Lowengrub, John S / Pathak, Medha M

    PLoS computational biology

    2024  Volume 20, Issue 4, Page(s) e1011855

    Abstract: The collective migration of keratinocytes during wound healing requires both the generation and transmission of mechanical forces for individual cellular locomotion and the coordination of movement across cells. Leader cells along the wound edge transmit ...

    Abstract The collective migration of keratinocytes during wound healing requires both the generation and transmission of mechanical forces for individual cellular locomotion and the coordination of movement across cells. Leader cells along the wound edge transmit mechanical and biochemical cues to ensuing follower cells, ensuring their coordinated direction of migration across multiple cells. Despite the observed importance of mechanical cues in leader cell formation and in controlling coordinated directionality of cell migration, the underlying biophysical mechanisms remain elusive. The mechanically-activated ion channel PIEZO1 was recently identified to play an inhibitory role during the reepithelialization of wounds. Here, through an integrative experimental and mathematical modeling approach, we elucidate PIEZO1's contributions to collective migration. Time-lapse microscopy reveals that PIEZO1 activity inhibits leader cell formation at the wound edge. To probe the relationship between PIEZO1 activity, leader cell formation and inhibition of reepithelialization, we developed an integrative 2D continuum model of wound closure that links observations at the single cell and collective cell migration scales. Through numerical simulations and subsequent experimental validation, we found that coordinated directionality plays a key role during wound closure and is inhibited by upregulated PIEZO1 activity. We propose that PIEZO1-mediated retraction suppresses leader cell formation which inhibits coordinated directionality between cells during collective migration.
    MeSH term(s) Cell Movement/physiology ; Keratinocytes ; Ion Channels
    Chemical Substances Ion Channels
    Language English
    Publishing date 2024-04-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2193340-6
    ISSN 1553-7358 ; 1553-734X
    ISSN (online) 1553-7358
    ISSN 1553-734X
    DOI 10.1371/journal.pcbi.1011855
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: PIEZO1-HaloTag hiPSCs: Bridging Molecular, Cellular and Tissue Imaging.

    Bertaccini, Gabriella A / Evans, Elizabeth L / Nourse, Jamison L / Dickinson, George D / Liu, Gaoxiang / Casanellas, Ignasi / Seal, Sayan / Ly, Alan T / Holt, Jesse R / Yan, Shijun / Hui, Elliot E / Panicker, Mitradas M / Upadhyayula, Srigokul / Parker, Ian / Pathak, Medha M

    bioRxiv : the preprint server for biology

    2023  

    Abstract: PIEZO1 channels play a critical role in numerous physiological processes by transducing diverse mechanical stimuli into electrical and chemical signals. Recent studies underscore the importance of endogenous PIEZO1 activity and localization in regulating ...

    Abstract PIEZO1 channels play a critical role in numerous physiological processes by transducing diverse mechanical stimuli into electrical and chemical signals. Recent studies underscore the importance of endogenous PIEZO1 activity and localization in regulating mechanotransduction. To enable physiologically and clinically relevant human-based studies, we genetically engineered human induced pluripotent stem cells (hiPSCs) to express a HaloTag fused to endogenous PIEZO1. Combined with super-resolution imaging, our chemogenetic approach allows precise visualization of PIEZO1 in various cell types. Further, the PIEZO1-HaloTag hiPSC technology allows non-invasive monitoring of channel activity via Ca
    Language English
    Publishing date 2023-12-23
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.12.22.573117
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Correction: Spatiotemporal dynamics of PIEZO1 localization controls keratinocyte migration during wound healing.

    Holt, Jesse R / Zeng, Wei-Zheng / Evans, Elizabeth L / Woo, Seung-Hyun / Ma, Shang / Abuwarda, Hamid / Loud, Meaghan / Patapoutian, Ardem / Pathak, Medha M

    eLife

    2022  Volume 11

    Language English
    Publishing date 2022-04-01
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.79034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mechanically activated ion channel Piezo1 modulates macrophage polarization and stiffness sensing.

    Atcha, Hamza / Jairaman, Amit / Holt, Jesse R / Meli, Vijaykumar S / Nagalla, Raji R / Veerasubramanian, Praveen Krishna / Brumm, Kyle T / Lim, Huy E / Othy, Shivashankar / Cahalan, Michael D / Pathak, Medha M / Liu, Wendy F

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 3256

    Abstract: Macrophages perform diverse functions within tissues during immune responses to pathogens and injury, but molecular mechanisms by which physical properties of the tissue regulate macrophage behavior are less well understood. Here, we examine the role of ... ...

    Abstract Macrophages perform diverse functions within tissues during immune responses to pathogens and injury, but molecular mechanisms by which physical properties of the tissue regulate macrophage behavior are less well understood. Here, we examine the role of the mechanically activated cation channel Piezo1 in macrophage polarization and sensing of microenvironmental stiffness. We show that macrophages lacking Piezo1 exhibit reduced inflammation and enhanced wound healing responses. Additionally, macrophages expressing the transgenic Ca
    MeSH term(s) Actins/metabolism ; Animals ; Biocompatible Materials/adverse effects ; Cells, Cultured ; Cellular Microenvironment/immunology ; Disease Models, Animal ; Feedback, Physiological ; Female ; Foreign-Body Reaction/immunology ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Macrophage Activation ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mechanotransduction, Cellular/immunology ; Mice ; Primary Cell Culture ; Subcutaneous Tissue/surgery ; Wound Healing/immunology
    Chemical Substances Actins ; Biocompatible Materials ; Ion Channels ; Piezo1 protein, mouse
    Language English
    Publishing date 2021-05-31
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-23482-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Spatiotemporal dynamics of PIEZO1 localization controls keratinocyte migration during wound healing.

    Holt, Jesse R / Zeng, Wei-Zheng / Evans, Elizabeth L / Woo, Seung-Hyun / Ma, Shang / Abuwarda, Hamid / Loud, Meaghan / Patapoutian, Ardem / Pathak, Medha M

    eLife

    2021  Volume 10

    Abstract: Keratinocytes, the predominant cell type of the epidermis, migrate to reinstate the epithelial barrier during wound healing. Mechanical cues are known to regulate keratinocyte re-epithelialization and wound healing; however, the underlying molecular ... ...

    Abstract Keratinocytes, the predominant cell type of the epidermis, migrate to reinstate the epithelial barrier during wound healing. Mechanical cues are known to regulate keratinocyte re-epithelialization and wound healing; however, the underlying molecular transducers and biophysical mechanisms remain elusive. Here, we show through molecular, cellular, and organismal studies that the mechanically activated ion channel PIEZO1 regulates keratinocyte migration and wound healing. Epidermal-specific
    MeSH term(s) Animals ; Cell Movement ; Female ; Ion Channels/genetics ; Ion Channels/metabolism ; Keratinocytes/physiology ; Male ; Mice ; Mice, Transgenic ; Signal Transduction ; Wound Healing/genetics
    Chemical Substances Ion Channels ; Piezo1 protein, mouse
    Language English
    Publishing date 2021-09-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.65415
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Piezo1 channels restrain regulatory T cells but are dispensable for effector CD4

    Jairaman, Amit / Othy, Shivashankar / Dynes, Joseph L / Yeromin, Andriy V / Zavala, Angel / Greenberg, Milton L / Nourse, Jamison L / Holt, Jesse R / Cahalan, Stuart M / Marangoni, Francesco / Parker, Ian / Pathak, Medha M / Cahalan, Michael D

    Science advances

    2021  Volume 7, Issue 28

    Abstract: T lymphocytes encounter complex mechanical cues during an immune response. The mechanosensitive ion channel, Piezo1, drives inflammatory responses to bacterial infections, wound healing, and cancer; however, its role in helper T cell function remains ... ...

    Abstract T lymphocytes encounter complex mechanical cues during an immune response. The mechanosensitive ion channel, Piezo1, drives inflammatory responses to bacterial infections, wound healing, and cancer; however, its role in helper T cell function remains unclear. In an animal model for multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we found that mice with genetic deletion of Piezo1 in T cells showed diminished disease severity. Unexpectedly, Piezo1 was not essential for lymph node homing, interstitial motility, Ca
    MeSH term(s) Animals ; Cell Differentiation ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Ion Channels/genetics ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis ; T-Lymphocytes, Regulatory ; Th1 Cells
    Chemical Substances Ion Channels ; Piezo1 protein, mouse
    Language English
    Publishing date 2021-07-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abg5859
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Myosin-II mediated traction forces evoke localized Piezo1-dependent Ca

    Ellefsen, Kyle L / Holt, Jesse R / Chang, Alice C / Nourse, Jamison L / Arulmoli, Janahan / Mekhdjian, Armen H / Abuwarda, Hamid / Tombola, Francesco / Flanagan, Lisa A / Dunn, Alexander R / Parker, Ian / Pathak, Medha M

    Communications biology

    2019  Volume 2, Page(s) 298

    Abstract: Piezo channels transduce mechanical stimuli into electrical and chemical signals to powerfully influence development, tissue homeostasis, and regeneration. Studies on Piezo1 have largely focused on transduction of "outside-in" mechanical forces, and its ... ...

    Abstract Piezo channels transduce mechanical stimuli into electrical and chemical signals to powerfully influence development, tissue homeostasis, and regeneration. Studies on Piezo1 have largely focused on transduction of "outside-in" mechanical forces, and its response to internal, cell-generated forces remains poorly understood. Here, using measurements of endogenous Piezo1 activity and traction forces in native cellular conditions, we show that cellular traction forces generate spatially-restricted Piezo1-mediated Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Signaling ; Cells, Cultured ; Fibroblasts/metabolism ; Humans ; Ion Channels/deficiency ; Ion Channels/genetics ; Ion Channels/metabolism ; Male ; Mechanotransduction, Cellular ; Mice, Knockout ; Myosin Type II/metabolism ; Neural Stem Cells/metabolism ; Time Factors
    Chemical Substances Ion Channels ; PIEZO1 protein, human ; Piezo1 protein, mouse ; Myosin Type II (EC 3.6.1.-) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2019-08-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Video-Audio Media
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-019-0514-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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