Signaling of mechanical stretch in XXXX keratinocytes via MAP kinases.

@entity1 @entity8652 @entity3963 @entity3962 @entity2733 @entity2393
Cells within @entity1 skin are permanently exposed to mechanical stretching. Here we present evidence that alterations in cell shape trigger biochemical signaling via MAP kinases in @entity1 keratinocytes. In an in vitro attempt we demonstrate a fast but transient activation of @entity3962 in response to cell stretch. This activation is reversed by preincubation with functional blocking antibodies directed towards @entity2393 . As a second member of MAP kinases, stress-activated protein kinase/c-JUN @entity2733 -terminal kinase was activated in a slower fashion, peaking at 1 h after the initial stimulus. The delay in signal transmission suggests that @entity3962 and stress-activated protein kinase/c-JUN @entity2733 -terminal kinase do not share the same signaling pathway. @entity3963 was not activated by cell stretching. The contribution of cytoskeletal elements in signal perception and transduction was evaluated by selective disruption of either actin filaments, microtubules, or keratin filaments but showed no clear effect on stretch-induced activation of @entity3962 and stress-activated protein kinase/c-JUN @entity2733 -terminal kinase. In conclusion we found evidence of a cell-shape-dependent activation of MAP kinases in @entity1 keratinocytes disclosing @entity8652 -integrins as putative mechano-transducers. It is likely that alterations of skin mechanics in vivo underlying pathogenic processes like wound formation and healing trigger physiologic responses via the MAP kinase pathway.
