Overexpression of Activin A in the Skin of Transgenic Mice Reveals New Activities in Epidermal Morphogenesis, Dermal Fibrosis, and Wound Repair

    October 1999 in “ EMBO journal
    Barbara Munz
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    TLDR Overexpression of activin A in mice skin causes skin thickening, fibrosis, and improved wound healing.
    The study demonstrated that overexpression of activin A in the skin of transgenic mice led to significant morphological changes, including smaller body size, smaller ears, shorter tails, and replacement of fatty tissue with connective tissue. The epidermis showed severe thickening and disorganization due to increased proliferation of basal keratinocytes and abnormal keratinocyte differentiation. After skin injury, these mice exhibited enhanced granulation tissue formation, likely due to premature induction of fibronectin and tenascin-C expression. These findings revealed new roles for activin in regulating keratinocyte proliferation, differentiation, dermal fibrosis, and wound repair.
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