A Role for TGF-β1-Induced Cellular Responses during Wound Healing of the Non-Scarring Early Human Fetus?
Autor: | Janette Richardson, Addie Grobbelaar, C. Vigor, Claire Linge, Kerstin J. Rolfe, Laurie Montgomery Irvine |
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Rok vydání: | 2007 |
Předmět: |
medicine.medical_treatment
Smad Proteins Dermatology Biology Biochemistry Collagen Type I Transforming Growth Factor beta1 Cicatrix Fetus medicine Humans Regeneration RNA Messenger Molecular Biology Cells Cultured Wound Healing Kinase Regeneration (biology) JNK Mitogen-Activated Protein Kinases Cell Differentiation Dermis Cell Biology Fibroblasts Cell biology Cytokine Immunology Signal transduction Wound healing Myofibroblast Transforming growth factor Signal Transduction |
Zdroj: | Journal of Investigative Dermatology. 127(11):2656-2667 |
ISSN: | 0022-202X |
DOI: | 10.1038/sj.jid.5700951 |
Popis: | Early human fetuses regenerate cutaneous wounds perfectly without scarring. However, transforming growth factor-beta1 (TGF-beta1), the cytokine linked with scarring in mature tissue, is also present during fetal wound repair, albeit transiently. We present a comparison of response to TGF-beta1 by fibroblasts derived from early human fetal skin (non-scarring) and their mature (scarring) postnatal counterparts, which revealed that although fetal fibroblasts do indeed differentiate into myofibroblasts, this response is altogether more rapid and short-lived. Fetal fibroblasts also failed to exhibit the TGF-beta1-induced increase in collagen (mRNA and protein) demonstrated by their postnatal counterparts. Fetal cells exhibited a comparatively short-lived or rapid phosphorylation of several components of the TGF-beta1 signaling pathways: Smad2/3 and c-Jun N-terminal kinase. Unlike quiescent postnatal fibroblasts, quiescent fetal fibroblasts also phosphorylated extracellular signal-regulated kinases in response to TGF-beta1. These altered responses to TGF-beta1 may well contribute to the transition between perfect regeneration and scar formation seen during development. |
Databáze: | OpenAIRE |
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