Human Amnion-Derived Cells for Neonatal Hypoxic-Ischemic Encephalopathy in Mice
摘要
The human amniotic membrane (hAM), a part of the fetal placenta, plays an essential role in fetal development by acting as a barrier and a site for metabolic and hormonal activity. Structurally, it consists of an epithelial cell layer supported by a mesenchymal stromal layer. From hAM, two stemlike cell types can be isolated: human amniotic epithelial cells (hAECs) and human amniotic mesenchymal stromal cells (hAM-MSCs). The hAECs, originating from the embryonic epiblast, express pluripotency markers such as Oct4, Nanog, and SSEA-4, indicating the capacity to differentiate into all three germ layers. The hAM-MSCs, derived from embryonic mesoderm, show mesenchymal characteristics and express markers like CD90 and CD105. Both cell types, but mainly the hAECs exhibit low immunogenicity, express nonclassical MHC molecules (HLA-G, HLA-E), and are non-tumorigenic—making them promising candidates for regenerative medicine. Recent preclinical studies suggest that the anti-inflammatory and neuroprotective effects of these cells may offer therapeutic benefits in neonatal hypoxic-ischemic encephalopathy (HIE), a serious brain injury resulting from perinatal oxygen deprivation. In this chapter, we describe experimental approaches in which hAECs or hAM-MSCs are transplanted into a neonatal mouse model of HIE to assess their potential for brain repair and functional recovery.