Artículos de revistas
Histatins, wound healing, and cell migration
Fecha
2017Registro en:
Oral Diseases, Volumen 24, Issue 7, 2017, Pages 1150-1160.
16010825
1354523X
10.1111/odi.12816
Autor
Torres, P.
Castro, M.
Reyes, M.
Torres, V.
Institución
Resumen
Wounds in the oral mucosa heal faster and more efficiently than those in the skin, although the mechanisms underlying these differences are not completely clear. In the
last 10 years, a group of salivary peptides, the histatins, has gained attention on behalf
of their ability to improve several phases of the wound-healing process. In addition to
their roles as anti-microbial agents and in enamel maintenance, histatins elicit other
biological effects, namely by promoting the migration of different cell types contained
in the oral mucosa and in non-oral tissues. Histatins, and specifically histatin-1, promote cell adhesion and migration in oral keratinocytes, gingival and dermal fibroblasts,
non-oral epithelial cells, and endothelial cells. This is particularly relevant, as histatin-1
promotes the re-epithelialization phase and the angiogenic responses by increasing
epithelial and endothelial cell migration. Although the molecular mechanisms associated with histatin-dependent cell migration remain poorly understood, recent studies
have pointed to the control of signaling endosomes and the balance of small GTPases.
This review aimed to update the literature on the effects of histatins in cell migration,
with a focus on wound healing. We will also discuss the consequences that this increasing field will have in disease and therapy design.