Abstract
The application of amniotic membrane (AM) on chronic wounds has proven very effective at resetting wound healing, particularly in re-epithelialization. Historically, several aspects of AM effect on wound healing have been evaluated using cell models. In keratinocytes, the presence of AM induces the activation of mitogen-activated protein (MAP) kinase and c-Jun N-terminal kinase (JNK) pathways, together with the high expression of c-Jun, an important transcription factor for the progression of the re-epithelialization tongue. In general, the levels of transforming growth factor (TGF)-β present in a wound are critical for the process of wound healing; they are elevated during the inflammation phase and remain high in some chronic wounds. Interestingly, the presence of AM, through epidermal growth factor (EGF) signaling, produces a fine-tuning of the TGF-β signaling pathway that re-conducts the stalled process of wound healing. However, the complete suppression of TGF-β signaling has proven negative for the AM stimulation of migration, suggesting that a minimal amount of TGF-β signaling is required for proper wound healing. Regarding migration machinery, AM contributes to the dynamics of focal adhesions, producing a high turnover and thus speeding up remodeling. This is clear because proteins, such as Paxillin, are activated upon treatment with AM. On top of this, AM also produces changes in the expression of Paxillin. Although we have made great progress in understanding the effects of AM on chronic wound healing, a long way is still ahead of us to fully comprehend its effects.
Highlights
A proper wound healing process in an orderly and timely manner is critical for skin restoration after injury
Keratinocyte motility is driven by rearrangements of the actin cytoskeleton to produce lamellipodia and filopodia, both of which adhere to the extracellular matrix (ECM) with the help of integrins and drag the cell forward (Mayor and Etienne-Manneville, 2016)
Wound fluid derived from diabetic foot and venous leg ulcers is rich in proinflammatory cytokines, such as TNF-α and IL1β; and transforming growth factor (TGF)-β (Harris et al, 1995; Jude et al, 2002)
Summary
A proper wound healing process in an orderly and timely manner is critical for skin restoration after injury This process involves four stages, whose progression overlaps, namely, hemostasis, inflammation, proliferation, and remodeling (Singer and Clark, 1999; Insausti et al, 2016; Castellanos et al, 2017). During the remodeling phase, wound contracts forming a scar involving ECM remodeling and apoptosis of fibroblasts and macrophages, once their function has been completed. Various factors, such as, age, diabetes, or large deep wounds, may lead to wound chronification with negative consequences, resulting in re-epithelialization failure (Figure 1). We will discuss identified signaling pathways in epithelial cells, involved at the cellular level, which prompt this AM-stimulated reepithelialization
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