Oxytocin deficiency impairs maternal skeletal remodeling.
We have reported that the posterior pituitary hormone, oxytocin (OT), known for its effects in inducing parturition, lactation and social bonding, is also a skeletal hormone. Here, we demonstrate that OT plays a key role in enabling maternal skeletal mobilization during pregnancy by enhancing the formation of bone resorbing osteoclasts. Osteoclast formation ex vivo is thus diminished in pregnant mothers with genetic OT-deficiency. OT(-/-) pups at day E20 also show a defect in trabecular bone. microCT measurements reveal normal bone volume, but increased trabecular numbers, suggesting that trabeculae in OT(-/-) pups are hypomineralized. We suggest that OT facilitates intergenerational transfer of calcium ions from a pregnant mother to the pups.
Liu
Xuan
X
Mount Sinai School of Medicine, NY, USA.
Shimono
Kengo
K
Zhu
Ling-Ling
LL
Li
Jianhua
J
Peng
Yuanzhen
Y
Imam
Aliza
A
Iqbal
Jameel
J
Moonga
Surinder
S
Colaianni
Graziana
G
Su
Cai
C
Lu
Zuhong
Z
Iwamoto
Masahiro
M
Pacifici
Maurizio
M
Zallone
Alberta
A
Sun
Li
L
Zaidi
Mone
M
D000818:Animals; D001842:Bone and Bones / Q000196:embryology* / Q000378:metabolism; D002113:Calcification, Physiologic / Q000235:genetics / Q000502:physiology*; D020013:Calcium Signaling; D005260:Female; D051379:Mice; D008817:Mice, Mutant Strains; D010010:Osteoclasts / Q000378:metabolism / Q000502:physiology*; D010121:Oxytocin / Q000235:genetics / Q000502:physiology*; D011247:Pregnancy
D010121:Oxytocin