Diabetes is a syndrome characterized by disordered metabolism and hyperglycemia, causing abnormalities of intrauterine metabolic and hormonal milieu during pregnancy, but there is little information about the influences of diabetes on growth factor and immune responses at the feto-maternal interface. Uterine natural killer (uNK) cells have role for immune responses at the feto-maternal in mice, and produce several cytokines and growth factors such as Vascular Endothelial Growth Factor (VEGF), VEGF is also responsible for development of the placenta and angiogenesis. Cysteine-rich heparin binding protein (type CRY61) has role during about vessel development in both the placenta and the embryo. Although, CYR61 can regulate the expression of genes involved in angiogenesis and matrix remodeling, including VEGF-A, VEGF-C, type I collagen, matrix metalloproteinase. Therefore, this objective study effect of diabetes and its impact on uNK cells, CYR61 and VEGF expression on day 12 and 14 of pregnant ICR mice. ICR mice were divided into two groups, the STZ group (Streptozotocin-induced diabetes mice with Type-I diabetes) and control mice (Sodium citrate buffer) The placenta was processed for Histological technical,stained by periodic acid Schiff (PAS) and the cell density (cells/mm2) of uNK cells was calculated in the metrial gland of each mouse model. The cell density of uNK cells in the metrial gland of STZ mice was not significantly when compared to control mice on Day 12 and 14 of pregnancy.On the other hand, cell density of uNK cells in control mice was significantly decreased on Day 14 of pregnancy when compared to Day 12 of pregnancy, while the uNk cell in STZ mice was no significantly on Day 12 of pregnancy whencompared to Day 14 of pregnancy. These results show that diabetes condition affected to persistence of uNk cells at Day 14 of pregnancy.