Walmsley Graham G, Hu Michael S, Hong Wan Xing, Maan Zeshaan N, Lorenz H Peter, Longaker Michael T
Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine.
Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine; Department of Surgery, John A. Burns School of Medicine, University of Hawai'i.
J Vis Exp. 2015 Jan 16(95):52297. doi: 10.3791/52297.
Early in utero, but not in postnatal life, cutaneous wounds undergo regeneration and heal without formation of a scar. Scarless fetal wound healing occurs across species but is age dependent. The transition from a scarless to scarring phenotype occurs in the third trimester of pregnancy in humans and around embryonic day 18 (E18) in mice. However, this varies with the size of the wound with larger defects generating a scar at an earlier gestational age. The emergence of lineage tracing and other genetic tools in the mouse has opened promising new avenues for investigation of fetal scarless wound healing. However, given the inherently high rates of morbidity and premature uterine contraction associated with fetal surgery, investigations of fetal scarless wound healing in vivo require a precise and reproducible surgical model. Here we detail a reliable model of fetal scarless wound healing in the dorsum of E16.5 (scarless) and E18.5 (scarring) mouse embryos.
在子宫内早期，而非出生后，皮肤伤口会进行再生且愈合时不会形成瘢痕。无瘢痕胎儿伤口愈合在所有物种中都会发生，但与年龄有关。从无瘢痕表型到瘢痕形成表型的转变在人类妊娠晚期发生，在小鼠中约在胚胎第18天（E18）发生。然而，这会因伤口大小而异，较大的缺损会在更早的胎龄产生瘢痕。小鼠中谱系追踪和其他基因工具的出现为胎儿无瘢痕伤口愈合的研究开辟了有前景的新途径。然而，鉴于胎儿手术本身具有较高的发病率和子宫过早收缩率，对胎儿无瘢痕伤口愈合的体内研究需要一个精确且可重复的手术模型。在此，我们详细介绍了一种可靠的胎儿无瘢痕伤口愈合模型，用于E16.5（无瘢痕）和E18.5（形成瘢痕）小鼠胚胎背部。
