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We are analyzing https://link.springer.com/article/10.1186/1471-2121-7-4.

Title:
Wnt signaling induces epithelial differentiation during cutaneous wound healing | BMC Molecular and Cell Biology
Description:
Background Cutaneous wound repair in adult mammals does not regenerate the original epithelial architecture and results in altered skin function. We propose that lack of regeneration may be due to the absence of appropriate molecular signals to promote regeneration. In this study, we investigated the regulation of Wnt signaling during cutaneous wound healing and the consequence of activating either the beta-catenin-dependent or beta-catenin-independent Wnt signaling on epidermal architecture during wound repair. Results We determined that the expression of Wnt ligands that typically signal via the beta-catenin-independent pathway is up-regulated in the wound while the beta-catenin-dependent Wnt signaling is activated in the hair follicles adjacent to the wound edge. Ectopic activation of beta-catenin-dependent Wnt signaling with lithium chloride in the wound resulted in epithelial cysts and occasional rudimentary hair follicle structures within the epidermis. In contrast, forced expression of Wnt-5a in the deeper wound induced changes in the interfollicular epithelium mimicking regeneration, including formation of epithelia-lined cysts in the wound dermis, rudimentary hair follicles and sebaceous glands, without formation of tumors. Conclusion These findings suggest that adult interfollicular epithelium is capable of responding to Wnt morphogenic signals necessary for restoring epithelial tissue patterning in the skin during wound repair.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Pets
  • Science

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,432 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

wound, wnt, skin, epithelial, hair, article, mice, pubmed, wounds, signaling, cells, expression, google, scholar, wnta, cas, pathway, cell, adult, normal, control, βcatenindependent, healing, activation, day, follicles, follicle, time, cutaneous, development, stem, βcatenin, retroviral, formation, tissue, βcateninindependent, days, repair, regeneration, epithelium, pmxwnta, cysts, signals, dermis, sebaceous, glands, activity, treated, original, topgal,

Topics {✒️}

pe-conjugated anti-cd5 antibody glycogen synthase kinase-3β pe-labeled anti-cd5 antibody β-catenin-dependent pathway depending β-catenin-independent signaling pathway β-catenin-dependent signaling shows inserted full-length wnt-5a mapping wnt/beta-catenin signaling β-catenin-independent wnt signaling beta-catenin-independent wnt signaling β-catenin-dependent wnt signaling β-catenin-dependent wnt pathway beta-catenin-dependent wnt signaling β-catenin-dependent pathway resulted beta-catenin signalling anti-β-catenin antibody activate β-catenin-independent signaling β-catenin/tcf-responsive promoter [13] open access article β-catenin-independent signaling β-catenin-independent pathway β-catenin-dependent signaling β-catenin-dependent signaling [12] sebaceous gland formation beta-catenin-independent pathway β-catenin-dependent pathway β-catenin dependent pathway β-catenin-dependent pathway [14] free cytosolic β-catenin β-catenin favored differentiation liquid nitrogen-cooled mortar β-galactosidase activity compared β-galactosidase reporter gene wnt signalling robust β-gal activity β-gal activity compared article download pdf β-catenin-independent wnts anterior-posterior axis formation bone marrow-derived cells high-efficiency gene transfer β-gal activity detected pmxwnt-5a treated wounds brian kim pre-selected wnt genes transparent semi-occlusive dressing pmxwnt-5a treated mice wnt-5a treated wounds collagen-rich dermal matrix male c57bl/6j mice

Questions {❓}

  • Korbling M, Estrov Z: Adult stem cells for tissue repair - a new therapeutic concept?
  • The histology of the observed cysts is similar to that seen in the ?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Wnt signaling induces epithelial differentiation during cutaneous wound healing
         description:Cutaneous wound repair in adult mammals does not regenerate the original epithelial architecture and results in altered skin function. We propose that lack of regeneration may be due to the absence of appropriate molecular signals to promote regeneration. In this study, we investigated the regulation of Wnt signaling during cutaneous wound healing and the consequence of activating either the beta-catenin-dependent or beta-catenin-independent Wnt signaling on epidermal architecture during wound repair. We determined that the expression of Wnt ligands that typically signal via the beta-catenin-independent pathway is up-regulated in the wound while the beta-catenin-dependent Wnt signaling is activated in the hair follicles adjacent to the wound edge. Ectopic activation of beta-catenin-dependent Wnt signaling with lithium chloride in the wound resulted in epithelial cysts and occasional rudimentary hair follicle structures within the epidermis. In contrast, forced expression of Wnt-5a in the deeper wound induced changes in the interfollicular epithelium mimicking regeneration, including formation of epithelia-lined cysts in the wound dermis, rudimentary hair follicles and sebaceous glands, without formation of tumors. These findings suggest that adult interfollicular epithelium is capable of responding to Wnt morphogenic signals necessary for restoring epithelial tissue patterning in the skin during wound repair.
         datePublished:2006-01-20T00:00:00Z
         dateModified:2006-01-20T00:00:00Z
         pageStart:1
         pageEnd:9
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1471-2121-7-4
         keywords:
            Hair Follicle
            Normal Skin
            Sebaceous Gland
            Cutaneous Wound
            Epithelial Cyst
            Cell Biology
            Biological Microscopy
            Life Sciences
            general
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         isPartOf:
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            issn:
               1471-2121
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                        name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
                        type:PostalAddress
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                     address:
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                        type:PostalAddress
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                     name:University of Washington School of Medicine
                     address:
                        name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
                        type:PostalAddress
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               name:Randall Moon
               affiliation:
                     name:University of Washington School of Medicine
                     address:
                        name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
                        type:PostalAddress
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               name:Frank Isik
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                        name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
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      context:https://schema.org
ScholarlyArticle:
      headline:Wnt signaling induces epithelial differentiation during cutaneous wound healing
      description:Cutaneous wound repair in adult mammals does not regenerate the original epithelial architecture and results in altered skin function. We propose that lack of regeneration may be due to the absence of appropriate molecular signals to promote regeneration. In this study, we investigated the regulation of Wnt signaling during cutaneous wound healing and the consequence of activating either the beta-catenin-dependent or beta-catenin-independent Wnt signaling on epidermal architecture during wound repair. We determined that the expression of Wnt ligands that typically signal via the beta-catenin-independent pathway is up-regulated in the wound while the beta-catenin-dependent Wnt signaling is activated in the hair follicles adjacent to the wound edge. Ectopic activation of beta-catenin-dependent Wnt signaling with lithium chloride in the wound resulted in epithelial cysts and occasional rudimentary hair follicle structures within the epidermis. In contrast, forced expression of Wnt-5a in the deeper wound induced changes in the interfollicular epithelium mimicking regeneration, including formation of epithelia-lined cysts in the wound dermis, rudimentary hair follicles and sebaceous glands, without formation of tumors. These findings suggest that adult interfollicular epithelium is capable of responding to Wnt morphogenic signals necessary for restoring epithelial tissue patterning in the skin during wound repair.
      datePublished:2006-01-20T00:00:00Z
      dateModified:2006-01-20T00:00:00Z
      pageStart:1
      pageEnd:9
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1471-2121-7-4
      keywords:
         Hair Follicle
         Normal Skin
         Sebaceous Gland
         Cutaneous Wound
         Epithelial Cyst
         Cell Biology
         Biological Microscopy
         Life Sciences
         general
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2121-7-4/MediaObjects/12860_2005_Article_177_Fig1_HTML.jpg
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1471-2121-7-4/MediaObjects/12860_2005_Article_177_Fig3_HTML.jpg
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            1471-2121
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         name:BioMed Central
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            type:ImageObject
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      author:
            name:Carrie Fathke
            affiliation:
                  name:University of Washington School of Medicine
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                     name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
                     type:PostalAddress
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                  address:
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                     type:PostalAddress
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            name:Kavita Shah
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                  name:University of Washington School of Medicine
                  address:
                     name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
                     type:PostalAddress
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            type:Person
            name:Brian Kim
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                  name:University of Washington School of Medicine
                  address:
                     name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
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                  type:Organization
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            name:Anne Hocking
            affiliation:
                  name:University of Washington School of Medicine
                  address:
                     name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Randall Moon
            affiliation:
                  name:University of Washington School of Medicine
                  address:
                     name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Frank Isik
            affiliation:
                  name:University of Washington School of Medicine
                  address:
                     name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
                     type:PostalAddress
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      name:BioMed Central
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      name:University of Washington School of Medicine
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         name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
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         name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
         type:PostalAddress
      name:University of Washington School of Medicine
      address:
         name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
         type:PostalAddress
      name:University of Washington School of Medicine
      address:
         name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
         type:PostalAddress
      name:University of Washington School of Medicine
      address:
         name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
         type:PostalAddress
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      address:
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      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Lynne Wilson
      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Kavita Shah
      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Brian Kim
      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Anne Hocking
      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Randall Moon
      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Frank Isik
      affiliation:
            name:University of Washington School of Medicine
            address:
               name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
      name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
      name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
      name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
      name:Department of Surgery, University of Washington School of Medicine, Seattle, USA
      name:Howard Hughes Medical Institute/Department of Pharmacology, University of Washington School of Medicine, Seattle, USA
      name:Department of Surgery, University of Washington School of Medicine, Seattle, USA

External Links {🔗}(148)

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