Connexins 26, 30, and 43: differences among spontaneous, chronic, and accelerated human wound healing.
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Connexins 26, 30, and 43: differences among spontaneous, chronic, and accelerated human wound healing. / Brandner, Johanna; Houdek, Pia; Hüsing, Birgit; Kaiser, Colette; Moll, Ingrid.
In: J INVEST DERMATOL, Vol. 122, No. 5, 5, 2004, p. 1310-1320.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Connexins 26, 30, and 43: differences among spontaneous, chronic, and accelerated human wound healing.
AU - Brandner, Johanna
AU - Houdek, Pia
AU - Hüsing, Birgit
AU - Kaiser, Colette
AU - Moll, Ingrid
PY - 2004
Y1 - 2004
N2 - Gap junctions (GJ) are known to be involved in spontaneous wound healing in rodent skin. We analyzed the staining patterns of the GJ proteins Cx26, Cx30, and Cx43 in human cutaneous wound healing and compared ex vivo spontaneous wound healing to non-healing wounds (chronic leg ulcers) and to ex vivo accelerated wound healing after transplantation of cultured keratinocytes. We demonstrate a loss of Cx43 staining at the wound margins during initial wound healing and after transplantation of keratinocytes. In contrast, Cx43 remains present at the margins of most non-healing wounds. We show a subsequent induction of Cx26 and Cx30 near the wound margins in spontaneous wound healing and-even earlier-after the transplantation of keratinocytes. The cells at the wound margins remain negative until the commencement of epidermal regeneration. Cx26/30 are present at the wound margins of most non-healing wounds. Cx stainings are absent in the transplanted keratinocytes during early wound healing, but there is a subsequent induction. Our results suggest that the downregulation of Cx43 is an important event in human wound healing. We discuss the assumption that direct cell-cell communication via GJ contribute to the acceleration of wound healing after the transplantation of keratinocytes.
AB - Gap junctions (GJ) are known to be involved in spontaneous wound healing in rodent skin. We analyzed the staining patterns of the GJ proteins Cx26, Cx30, and Cx43 in human cutaneous wound healing and compared ex vivo spontaneous wound healing to non-healing wounds (chronic leg ulcers) and to ex vivo accelerated wound healing after transplantation of cultured keratinocytes. We demonstrate a loss of Cx43 staining at the wound margins during initial wound healing and after transplantation of keratinocytes. In contrast, Cx43 remains present at the margins of most non-healing wounds. We show a subsequent induction of Cx26 and Cx30 near the wound margins in spontaneous wound healing and-even earlier-after the transplantation of keratinocytes. The cells at the wound margins remain negative until the commencement of epidermal regeneration. Cx26/30 are present at the wound margins of most non-healing wounds. Cx stainings are absent in the transplanted keratinocytes during early wound healing, but there is a subsequent induction. Our results suggest that the downregulation of Cx43 is an important event in human wound healing. We discuss the assumption that direct cell-cell communication via GJ contribute to the acceleration of wound healing after the transplantation of keratinocytes.
M3 - SCORING: Zeitschriftenaufsatz
VL - 122
SP - 1310
EP - 1320
JO - J INVEST DERMATOL
JF - J INVEST DERMATOL
SN - 0022-202X
IS - 5
M1 - 5
ER -