Disruption of the Cx43/miR21 pathway leads to osteocyte apoptosis and increased osteoclastogenesis with aging

DAVIS HM; PACHECO-COSTA R; ATKINSON EG; BRUN LR; GORTAZAR AR; HARRIS J; HIASA M; BOLARINWA SA; YONEDA T; IVAN M; BRUZZANITI A; BELLIDO T; PLOTKIN LI

AGING CELL

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2017 vol. 16 p. 551 - 551

1474-9718

!--[if gte mso 9]> Skeletal aging results in apoptosis ofosteocytes, cells embedded in bone that control the generation/function of boneforming and resorbing cells. Aging also decreases connexin43 (Cx43) expression inbone; and osteocytic Cx43 deletion partially mimics the skeletal phenotype of oldmice. Particularly, aging and Cx43 deletion increase osteocyte apoptosis, and osteoclastnumber and bone resorption on endocortical bone surfaces. We examined hereinthe molecular signaling events responsible for osteocyte apoptosis andosteoclast recruitment triggered by aging and Cx43 deficiency. Cx43-silenced MLO-Y4osteocytic (Cx43def) cells undergo spontaneous cell death in culturethrough caspase3 activation and exhibit increased levels of apoptosis-relatedgenes, and only transfection of Cx43 construc