Interferon tau: Influences on growth and development of the conceptus
- Additional Document Info
- View All
Interferon tau (IFNT), the pregnancy recognition signal secreted from trophectoderm cells of ruminant conceptuses abrogates the uterine luteolytic mechanism to ensure maintenance of functional corpora lutea for production of progesterone (P4). Importantly, IFNT, in concert with P4, also induces expression of genes in uterine luminal (LE) and superficial glandular (sGE) epithelia for transport and/or secretion of histotroph into the uterine lumen to support growth and development of the conceptus. For example, IFNT and P4 induce transporters responsible foer transport of glucose and arginine into the uterine lumen during the peri-implantation period of pregnancy. Arginine activates the mechanistic target of rapamycin (MTOR) nutrient sensing cell signaling pathway to stimulate proliferation, migration, differentiation and translation of mRNAs essential for growth and development of the conceptus. Glucose not utilized by the conceptus is converted to fructose and those two hexose sugars are metabolized via aerobic glycolysis to produce metabolites used in the hexosamine biosynthesis pathway, pathways for one-carbon metabolism, and pentose phosphate pathway for synthesis of ribose sugars and NADPH. Arginine is metabolized to nitric oxide (NO) that stimulates angiogenesis in uterine and placental tissues, and to polyamines required for many cellular functions critical for growth and development of the conceptus. In summary, IFNT and P4 regulate expression of genes for transport of select nutrients into the pregnant uterus during the peri-implantation period of pregnancy. Those nutrients are then metabolized via multiple metabolic pathways to not only provide ATP, but also substrates for synthesis of nucleotides, amino acids, co-factors required for growth, development, and survival of conceptuses during the peri-implantation period of pregnancy.
author list (cited authors)
Bazer, F. W., Seo, H., Wu, G., & Johnson, G. A.