Fetal parathyroids are not required to maintain placental calcium transport

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

“…1 ]. These data demonstrate that the fetomaternal calcium gradient in these mice is established between E17 and E19, and further suggest that active transplacental calciumtransport mechanisms during this period begin to contribute significantly to maternofetal calcium flux, consistent with other studies in mice and rats (23)(24)(25)(26). In contrast, fetal blood [Ca 2+ ] in P0 was significantly lower than WT and maternal blood at both E17 and E19 (P < 0.05).…”

“…Therefore, despite the marked growth restriction of the P0 fetuses at both E17 and E19 and a reduced placental mass, skeletal hypomineralization of the P0 fetus at E17 is corrected by E19, and this is achieved by a rise in Ca J mf . Work from several species suggests that active placental calcium transport is switched on, or up-regulated, near to term, as bone mineral accretion begins (23,25,26,(40)(41)(42)(43). The capacity to raise Ca J mf in P0 indicates that the functional integrity of active calcium-transport mechanisms in P0 placentas is preserved.…”

“…The fetal "demand" signals to elicit these changes in placental function remain to be fully elucidated, but are likely to be multifactorial. As regards placental calcium transport, the increasingly well-described role of parathyroid hormone-related peptide in regulating placental calcium transport (23,25,26,43) suggests one attractive candidate. This finding again highlights the potential role of the IPYS in the regulation of placental calcium transport, as both the PTH/PTHrP receptor and PTHrP are known to be highly expressed within the IPYS (21).…”

Relevance of the plasma membrane calcium-ATPase in the homeostasis of calcium in the fetal liver

“…In studies of mice deficient for Hoxa3, a transcription factor involved in parathyroid organogenesis, an absence of parathyroid glands and therefore PTH, were observed. 11 As a result, low calcium levels have been detected in both blood and amniotic fluid samples, while serum levels of PTHrP and the placental transport of calcium remained unaffected. In combination with studies of Pthrp -/-mutants, where serum PTHrP levels were found to increase concomitant with its overexpression in the liver and placenta, these findings suggest that these organs play active roles in fetal calcium homeostasis mediated by PTHrP instead of PTH.…”

“…In combination with studies of Pthrp -/-mutants, where serum PTHrP levels were found to increase concomitant with its overexpression in the liver and placenta, these findings suggest that these organs play active roles in fetal calcium homeostasis mediated by PTHrP instead of PTH. 11 On the other hand, several Ca 2C mobilizing systems are located in the plasma membrane and cytosolic organelles of hepatic cells, also working to maintain very low levels of calcium. In the plasma membrane of hepatocytes, the plasma membrane calcium ATPase (PMCA) is primarily responsible for maintaining low levels of calcium, since under normal conditions, the Na C /Ca 2C exchanger appears to be inactive.…”