The clinical significance and impact of interleukin 15 on keratinocyte cell growth and migration

A. M. Jones, J. L. Griffiths, A. J. Sanders, S. Owen, F. Ruge, K. G. Harding, W. G. Jiang*

*Awdur cyfatebol y gwaith hwn

Allbwn ymchwil: Cyfraniad at gyfnodolynErthygladolygiad gan gymheiriaid

11 Wedi eu Llwytho i Lawr (Pure)


Chronic wounds represent a significant burden to health services and are associated with patient morbidity. Novel methods to diagnose and/or treat problematic wounds are needed. Interleukin (IL)-15 is a cytokine involved in a number of biological processes and disease states such as inflammation, healing and cancer progression. The current study explores the expression profile of IL-15 and IL-15 receptor (IL-15R alpha) in chronic wounds and its impact on keratinocytes. IL-15 and IL-15R expression were examined in healing and non-healing chronic wounds using qPCR and immunohistochemical analysis. The impact of recombinant IL-15 (rhIL-15) on human adult low calcium temperature (HaCaT) keratinocyte growth and migratory potential was further examined. IL-15 transcript expression was slightly, though non-significantly elevated in healing chronic wounds compared with non-healing chronic wounds. IL-15 protein staining was minimal in both subtypes of chronic wounds. By contrast, IL-15R alpha transcript and protein expression were both observed to be enhanced in non-healing chronic wounds compared with healing chronic wounds. The treatment of HaCaT cells with rhIL-15 generally enhanced cell growth and promoted migration. Analysis with small molecule inhibitors suggested that the pro-migratory effect of rhIL-15 may be associated with ERK, AKT, PLC gamma and FAK signalling. IL-15 may promote healing traits in keratinocytes and the differential expression of IL-15R alpha is observed in chronic wounds. Together, this may imply a complex role for this interleukin in wound healing.

Iaith wreiddiolSaesneg
Tudalennau (o-i)679-686
Nifer y tudalennau8
CyfnodolynInternational Journal of Molecular Medicine
Rhif cyhoeddi3
Dynodwyr Gwrthrych Digidol (DOIs)
StatwsCyhoeddwyd - Medi 2016
Cyhoeddwyd yn allanolIe

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