Modification of collagen by 3-deoxyglucosone alters wound healing through differential regulation of p38 MAP kinase.

ABSTRACT:

Background

Wound healing is a highly dynamic process that requires signaling from the extracellular matrix to the fibroblasts for migration and proliferation, and closure of the wound. This rate of wound closure is impaired in diabetes, which may be due to the increased levels of the precursor for advanced glycation end products, 3-deoxyglucosone (3DG). Previous studies suggest a differential role for p38 mitogen-activated kinase (MAPK) during wound healing; whereby, p38 MAPK acts as a growth kinase during normal wound healing, but acts as a stress kinase during diabetic wound repair. Therefore, we investigated the signaling cross-talk by which p38 MAPK mediates wound healing in fibroblasts cultured on native collagen and 3DG-collagen.

Methodology/principal findings

Using hu

SUBMITTER: Loughlin DT 

PROVIDER: S-EPMC3089600 | biostudies-literature | 2011 May

REPOSITORIES: biostudies-literature