Expression of IGR-IR and VEGF and trophoblastic proliferative activity in placentas from pregnancies complicated by IUGR.
Intrauterine growth retardation (IUGR) is recognized as an important cause of low birth weight and elective preterm delivery. IUGR is associated with multiple causative factors, including placental dysfunction. The aim of this prospective study was to investigate the role of trophoblastic proliferative activity and type I insuline-like growth factor receptor (IGF-IR) and vascular endothelial growth factor (VEGF) expressions in the pathogenesis of IUGR. Immunohistochemistry using VEGF, IGF-IR, and Ki-67 antibodies was performed on formalin-fixed placental tissues of third-trimester pregnancies complicated by IUGR (n = 19) and pregnancies with appropriately grown fetuses (n = 27). In addition, histopathological examination of the placentas was performed, and histological findings were categorized into three groups: utero-placental vascular pathologies (UPVP), coagulation-related pathologies, and chronic inflammation. Statistical analysis revealed that villous trophoblastic IGF-IR immunostaining was significantly weaker in placentas with IUGR (p < 0.001), whereas trophoblastic Ki-67 proliferative index and VEGF immunoscoring did not show any significant difference. Histologically, UPVP and chronic inflammation were significant findings in placentas with IUGR (p = 0.04 and p = 0.04, respectively). In addition, placentas were significantly smaller in the IUGR group (p < 0.001). We conclude that villous trophoblastic IGF-IR expression may play a significant role in the pathogenesis of IUGR, and histopathological examination of placentas in pregnancies complicated by IUGR may yield significant findings. In contrast, based on our findings, trophoblastic proliferation and VEGF expression are unlikely to be significant parameters in the pathogenesis of IUGR.
Gurel
Duygu
D
Department of Pathology, School of Medicine, Dokuz Eylul University, Izmir, Turkey.
Ozer
Erdener
E
Altunyurt
Sabahattin
S
Guclu
Serkan
S
Demir
Namik
N
D000328:Adult; D002455:Cell Division; D002908:Chronic Disease; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D007231:Infant, Newborn; D007249:Inflammation; D019394:Ki-67 Antigen / Q000378:metabolism; D010920:Placenta / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D010922:Placenta Diseases / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011446:Prospective Studies; D017526:Receptor, IGF Type 1 / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
D019394:Ki-67 Antigen; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D017526:Receptor, IGF Type 1