Gestational changes in calbindin-D9k in rat uterus, yolk sac, and placenta: implications for maternal-fetal calcium transport and uterine muscle function.

Abstract

Calbindin-Dgk was quantified and its cellular location was defined in uterus, yolk sac, and placenta. In late gestation (days 17 to term) coordinated induction of calbindinDqk was seen in uterine epithelial lining cells and the juxtaposed yolk sac visceral epithelium as well as the intraplacental yolk sac epithelium. The induction of calbindin-Dk in these cells coincided with the time of exponential fetal bone growth and maximal fetal accumulation of calcium, suggesting a role of the protein in these epithelial layers in maternal-fetal calcium transport. Dynamic changes also occurred in the calbindin-Dgk contents of the two layers of uterine smooth muscle (outer longitudinal and inner circular) during mid-and late gestation.

Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

“…It should also be commented upon that although placental calbindin-D 9K expression is reduced in P0 at E17, the cellular origin of this response is uncertain, with a relatively high abundance of both calbindin-D 9K and PMCA within the mouse IPYS, along with calcitropic hormomes and receptors, providing a potential maternofetal calcium-transfer pathway in addition to exchange across the labyrinth trophoblast (21,22). Considering the marked induction in placental calbindin-D 9K expression in the IPYS toward term (39), one may suggest that any reduction in calbindin-D 9K expression within the IPYS of P0 placentas at E17 would have significant effects on fetal calcium accretion. Certainly, the relative contributions of the IPYS and labyrinthine trophoblasts toward this reduced calbindin-D 9K expression is worthy of further investigation.…”

Placental nutrient supply and fetal growth

“…Data suggest that in the mouse and rat placenta, as in other epithelia, Ca 2+ transport is likely to involve three main steps (Atkinson et al, 2006;Belkacemi et al, 2005): firstly, diffusion into the trophoblast from maternal plasma down an electrochemical gradient through epithelial Ca 2+ channels of the transient receptor potential (TRP) gene family; secondly, transfer across the trophoblast cytoplasm bound to the calcium binding protein calbindin-D 9K (Glazier et al, 1992); and, thirdly, active extrusion into the fetal compartment via plasma membrane Ca 2+ -ATPase (PMCA) localized to the BM (Borke et al, 1989;Fisher et al, 1987). Over the last third of gestation, gene and protein expression for calbindin-D 9K increases markedly in both mouse and rat placenta Glazier et al, 1992;Hamilton et al, 2000;Mathieu et al, 1989) and correlates with the increase in unidirectional maternofetal 45 Ca clearance measured over the same period (Glazier et al, 1992), suggesting that transcytosolic transfer on this protein and the dynamic equilibrium between bound and free Ca 2+ in the syncytiotrophoblast might be the rate limiting step of transfer in these species. The situation may well be quite different in the human placenta where it has proved difficult to show the expression of calbindin-D 9K (Belkacemi et al, 2004), or to determine if another protein is involved instead.…”

Molecular cloning of the full‐length cDNA encoding the human calbindin‐D9k

“…The CaBP-9k belongs to a family of calcium-binding proteins which includes such proteins as ealmodulin, parvalbumin, troponin C, and S100 protein [2]. CaBP-9k is found in the mammalian intestine [3]~ placenta [4], uterus [5], and kidney [6]. Its exact function is unknown.…”