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Model for re-epithelialisation of incisional wounds by normal and β1-null keratinocytes. Model for re-epithelialisation of incisional wounds by normal.

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Presentation on theme: "Model for re-epithelialisation of incisional wounds by normal and β1-null keratinocytes. Model for re-epithelialisation of incisional wounds by normal."— Presentation transcript:

1 Model for re-epithelialisation of incisional wounds by normal and β1-null keratinocytes.
Model for re-epithelialisation of incisional wounds by normal and β1-null keratinocytes. In skin of control mice, β1 integrins are localised to the basolateral surfaces of basal keratinocytes. After wounding, control keratinocytes use β1 integrins to bind to the newly exposed dermal ligands. Thus, re-epithelialisation occurs rapidly and results in a downward migration of the epidermis. In K5β1-null mice, keratinocytes are unable to recognise dermal ligands after wounding and remain static at the wound margin, although they still proliferate. Their cell-cell contacts are also tighter than those of control keratinocytes. Once the wound is filled with granulation tissue, which contains matrix molecules recognised by non-β1 integrins, K5β1-null keratinocytes are able to migrate across the surface of the wound to complete re-epithelialisation, but they do not show the V-shaped repair morphology characteristic of control wounds. Richard Grose et al. Development 2002;129: © 2002.


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