Cell and molecular mechanisms of keratinocyte function stimulated by insulin during wound healingReport as inadecuate

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BMC Cell Biology

, 10:1

First Online: 12 January 2009Received: 05 September 2008Accepted: 12 January 2009


BackgroundRegenerative wound repair is a goal of modern medicine. This is important not only for the local repair but also for its beneficial effect to systemic physiological processes. When wounds become chronic, individuals are susceptible to generalized inflammatory cascades that can affect many organs and even lead to death. Skin is the most commonly injured tissue, and its proper repair is important for reestablishment of its barrier function.

ResultsWe show here that insulin, when topically applied to skin excision wounds, accelerates re-epithelialization and stimulates -maturation- of the healing tissue. These effects are dependent on the insulin receptor but independent of EGF-EGF-R; PI3K-Akt-Rac1 signaling pathways are critically involved, and healing is α3 and LN332-dependent.

ConclusionInsulin has great potential for the treatments of chronic wounds in which re-epthelialization is impaired. Understanding of the pathways induced by insulin is important for the development of analog molecules that function strictly in healing. Because of its long history of safe use in humans for decades, this protein may prove to be a powerful therapy without major adverse effects.

AbbreviationsBMbasement membrane

CAconstitutively active

DNdominant negative

WTwild type

LN332laminin 332

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2121-10-1 contains supplementary material, which is available to authorized users.

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Author: Yan Liu - Melissa Petreaca - Min Yao - Manuela Martins-Green

Source: https://link.springer.com/article/10.1186/1471-2121-10-1

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