Premium
Growth promoting effects of human placental lactogen during early organogenesis: a link to insulin‐like growth factors
Author(s) -
KAGAN KARABULUT AHMET,
LAYFIELD ROBERT,
PRATTEN MARGARET K.
Publication year - 2001
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1046/j.1469-7580.2001.19860651.x
Subject(s) - placental lactogen , human placental lactogen , endocrinology , medicine , insulin , biology , somatomedin , embryo , embryogenesis , hormone , growth factor , embryonic stem cell , growth hormone , placenta , microbiology and biotechnology , fetus , pregnancy , biochemistry , receptor , genetics , gene
Many maternally derived factors may be involved in the regulation of embryonic growth but the control mechanisms involved are poorly understood. Human placental lactogen (hPL) has been implicated in playing a role in the control of embryonic growth. Several investigators suggested that there may be a possible link between the effects of this hormone and insulin‐like growth factors (IGFs). In order to determine the growth promoting potential of hPL and involvement of IGFs in the mechanism of action of the hormone, 9.5 d rat embryos were cultured in vitro for 48 h in depleted serum in the presence and absence of hPL with additional IGF antisera. The growth supporting capacity of the serum was reduced by removal of low molecular weight molecules by prolonged filtration of the serum using filters with a molecular weight exclusion of 30 kDa. Addition of hPL (3.2–25.6 ng/ml) to depleted serum significantly improved embryonic growth and development, suggesting that the developing embryo may utilise hPL. The presence of antisera against hPL, IGF‐I and ‐II abolished the hPL‐induced increase in the development in all parameters suggesting that there may be a possible link between the IGFs and the effects of hPL on rat embryonic development and this hormone may achieve its growth promoting effects via IGFs.