Bighorn sheep rams participate in high impact head-butting without overt signs of brain injury, thus providing a naturally occurring animal model for studying brain injury mitigation. Previously published finite element modeling showed that both the horn and bone materials play important roles in reducing brain cavity accelerations during ramming.
Heterozygous deletion of both sclerostin (Sost) and connexin43 (Gja1) genes in mice is not sufficient to impair cortical bone modeling
Connexin43 (Cx43) is the main gap junction protein expressed in bone forming cells, where it modulates peak bone mass acquisition and cortical modeling. Genetic ablation of the Cx43 gene (Gja1) results in cortical expansion with accentuated periosteal bone formation associated with decreased expression of the Wnt inhibitor sclerostin.
Defective signaling, osteoblastogenesis and bone remodeling in a mouse model of connexin 43 C-terminal truncation
In skeletal tissue, loss or mutation of the gap junction protein connexin 43 (Cx43, also known as GJA1) in cells of the osteoblast lineage leads to a profound cortical bone phenotype and defective tissue remodeling. There is mounting evidence in bone cells that the C-terminus (CT) of Cx43 is a docking platform for signaling effectors and is required for efficient downstream signaling.