Expression of insulin-like growth factor in the placenta of intrauterine growth-retarded human fetuses

DALÇIK H., YARDIMOĞLU M., VURAL B., DALÇIK C., FILIZ S., GONCA S., ...Daha Fazla

ACTA HISTOCHEMICA, cilt.103, sa.2, ss.195-207, 2001 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 103 Sayı: 2
  • Basım Tarihi: 2001
  • Doi Numarası: 10.1078/0065-1281-00580
  • Dergi Adı: ACTA HISTOCHEMICA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.195-207
  • Anahtar Kelimeler: insulin-like growth factor, intrauterine growth retardation, human placenta, IGF-BINDING PROTEIN-1, HUMAN-FETAL TISSUES, FACTOR-I, HORMONE-VARIANT, GENE-EXPRESSION, MESSENGER-RNAS, RECEPTORS, LOCALIZATION, TERM, RAT
  • İstanbul Üniversitesi Adresli: Hayır

Özet

Many cases of intrauterine growth retardation (IUGR) are the result of placental and fetal tissue insufficiency. Insulin-like growth factor-I (IGF-I) is known to play a role in placental and fetal growth. An immunocytochemical study was performed to localize ICF-I peptides in human placenta and umbilical cords of normal (n = 3) and IUGR (n = 3) fetuses. The peripartum fetal conditions were evaluated as well. Immunoreactive IGF-I was detected in the cytotrophoblast, syncytiotrophoblast, amnion, endothelial cells of fetal capillaries and in the decidua in both normal and IUGR placental tissue. A more robust immunostaining and increased numbers of positively stained cells were found in the decidua of IUGR placenta (p < 0.001). Intense immunostaining was also found in endothelial cells, smooth muscle cells and fibroblasts of the umbilical vein. IGF-I immunoreactivity was also present in stroma (Hofbauer cells and/or fibroblasts) of IUGR villi; Our results indicate that expression of IGF-I is high in specific sites in placenta and umbilical cords, which indicates a paracrine and/or endocrine function. The increased expression of IGF-I in placenta of IUGR fetuses indicates its involvement in restoring normal growth by means of a positive feed-back mechanism.