%0 Journal Article
%T Fetal Wound Healing Biomarkers
%A Fernanda Rodrigues Helmo
%A Juliana Reis Machado
%A Camila Souza de Oliveira Guimar£¿es
%A Vicente de Paula Antunes Teixeira
%A Marlene Ant£¿nia dos Reis
%A Rosana Rosa Miranda Corr¨ºa
%J Disease Markers
%D 2013
%R 10.1155/2013/567353
%X Fetal skin has the intrinsic capacity for wound healing, which is not correlated with the intrauterine environment. This intrinsic ability requires biochemical signals, which start at the cellular level and lead to secretion of transforming factors and expression of receptors, and specific markers that promote wound healing without scar formation. The mechanisms and molecular pathways of wound healing still need to be elucidated to achieve a complete understanding of this remodeling system. The aim of this paper is to discuss the main biomarkers involved in fetal skin wound healing as well as their respective mechanisms of action. 1. The Human Skin The skin is the largest organ of the human body and is responsible for the maintenance of homeostasis, hemodynamic control, sensory reception, and innate and adaptive immunity. The skin is divided into two layers: the epidermis and the dermis. The epidermis originates from the ectoderm and it is formed by different cell types. The dermis is derived from the mesoderm and is rich in dense connective tissues [1]. During embryonic development, the epidermis changes from a single layer of ectodermal cells at 7-8 days of gestation into a stratified, keratinized epithelium at 22¨C24 weeks of pregnancy [2]. Formation of hair follicles starts in the eighth week, and in the 12th week, the development of embryonic fibroblasts is organized in networks of collagen fibers [3, 4]. Type I collagen is the main component of the extracellular matrix (ECM) [5, 6] and it confers tensile strength [6]. Type I and type III collagen fibers are present in the fetal skin, and dermal fibroblast populations exhibit greater type I collagen compared to type III collagen staining [5]. Subsequently, the production of elastin by human skin fibroblasts increased from 7-fold to 14-fold between 17 and 19 weeks of pregnancy, reaching the levels found in neonatal skin fibroblasts [7]. The elastic tissue contributes to the structure of the fetal dermis and increases in quantity and complexity during intrauterine development [7]. With the advancement of the pregnancy, the number of epidermal cell layers increases and the hair follicles and sweat glands complete their maturation [8]. Fetal skin development is completed 30 weeks after conception [3, 9]. The complex maturation of human skin during fetal development is achieved by the action of chemical mediators. The organization and function of this organ may be compromised by numerous diseases or secondary mechanisms that lead to the loss of tissue continuity. The knowledge and understanding of the
%U http://www.hindawi.com/journals/dm/2013/567353/