Distinct roles of JNK-1 and ERK-2 isoforms in permeability barrier repair and wound healing
Autor: | Thomas Herdegen, Michael Schunck, Kirsten Mielke, Ehrhardt Proksch, Kathrin Koehler, Claudia Neumann |
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Rok vydání: | 2011 |
Předmět: |
MAPK/ERK pathway
Gene isoform Histology MAP Kinase Signaling System Permeability Pathology and Forensic Medicine Mice Immune system In vivo medicine Animals Humans Mitogen-Activated Protein Kinase 8 Skin Mitogen-Activated Protein Kinase 1 Wound Healing integumentary system biology Kinase Cell Biology General Medicine Cell biology medicine.anatomical_structure Mitogen-activated protein kinase biology.protein Keratinocyte Wound healing |
Zdroj: | European Journal of Cell Biology. 90:565-571 |
ISSN: | 0171-9335 |
DOI: | 10.1016/j.ejcb.2010.10.017 |
Popis: | c-Jun N-terminal kinases (JNKs, also called stress activated protein kinases) and the extra-cellular signal responsive kinases (ERKs) exert different functions in mitogenesis, maturation and differentiation of immune and epithelial cells. We investigated specific functions of individual JNK and ERK isoforms in skin permeability barrier repair and in wound healing. JNK1, but not JNK2 or JNK3, deficient mice revealed a delay in the permeability barrier repair after superficial injury to the skin (tape-stripping) as well as a delay in the healing of full skin thickness wounds. Skin barrier injury induced an increase in epidermal JNK1 enzyme activity in mouse skin in vivo, and JNK1 activity correlated with the degree of differentiation in organotypic keratinocyte cultures. Skin injury activated epidermal ERK2 enzyme activity with biphasic maxima after 30 min and 3h, and the activity was independent from the differentiation state in keratinocyte culture. In summary, superficial and deep wound healing depends on the differential activity of MAP kinases such as JNK1 in epidermal differentiation and ERK2 in proliferation. |
Databáze: | OpenAIRE |
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