PMID- 14989492
OWN - NLM
STAT- MEDLINE
DCOM- 20040907
LR  - 20091119
IS  - 0344-0338 (Print)
IS  - 0344-0338 (Linking)
VI  - 199
IP  - 12
DP  - 2003
TI  - Expression of IGR-IR and VEGF and trophoblastic proliferative activity in 
      placentas from pregnancies complicated by IUGR.
PG  - 803-9
AB  - 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.
FAU - Gurel, Duygu
AU  - Gurel D
AD  - Department of Pathology, School of Medicine, Dokuz Eylul University, Izmir, 
      Turkey.
FAU - Ozer, Erdener
AU  - Ozer E
FAU - Altunyurt, Sabahattin
AU  - Altunyurt S
FAU - Guclu, Serkan
AU  - Guclu S
FAU - Demir, Namik
AU  - Demir N
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Pathol Res Pract
JT  - Pathology, research and practice
JID - 7806109
RN  - 0 (Ki-67 Antigen)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 2.7.10.1 (Receptor, IGF Type 1)
SB  - IM
MH  - Adult
MH  - Cell Division
MH  - Chronic Disease
MH  - Female
MH  - Fetal Growth Retardation/etiology/*metabolism/pathology
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - Infant, Newborn
MH  - Inflammation
MH  - Ki-67 Antigen/metabolism
MH  - Placenta/blood supply/*metabolism/pathology
MH  - Placenta Diseases/metabolism/pathology
MH  - Pregnancy
MH  - Prospective Studies
MH  - Receptor, IGF Type 1/*metabolism
MH  - Vascular Endothelial Growth Factor A/*metabolism
EDAT- 2004/03/03 05:00
MHDA- 2004/09/08 05:00
CRDT- 2004/03/03 05:00
PHST- 2004/03/03 05:00 [pubmed]
PHST- 2004/09/08 05:00 [medline]
PHST- 2004/03/03 05:00 [entrez]
AID - S0344-0338(04)70497-5 [pii]
AID - 10.1078/0344-0338-00499 [doi]
PST - ppublish
SO  - Pathol Res Pract. 2003;199(12):803-9. doi: 10.1078/0344-0338-00499.