At puberty, oestrogen promotes skeletal maturation and the gradual, progressive closure of the epiphyseal growth plate, possibly as a consequence of both oestrogen - induced vascular and osteoplastic invasion and the termination
of chondrogenesis.
Comparison
of chondrogenesis in static and dynamic environments using a SFF designed and fabricated PCL - PEO scaffold.
Cartilage formation (chondrogenesis) requires the normal function of Sox9, a protein that regulates the expression
of chondrogenesis - related genes.
Not exact matches
By contrast, the R206H ACVR1 mutant only slightly enhances the expression
of initial and early
chondrogenesis markers (collagen type II and aggrecan), consistent with a milder stimulatory effect
of the FOP ACVR1 mutation on chondrocyte differentiation.
The condensation phase
of mesenchymal prechondrogenic cells is the first event in
chondrogenesis, characterized by the expression
of collagen type II (44).
Remarkably, the relative expression levels
of all marker genes were only slightly decreased when R206H ACVR1 and Q207D caACVR1 cultures were cotransfected with Noggin, whereas cells expressing the wild - type ACVR1 or empty viral vector showed clear downregulation
of all analyzed marker genes for
chondrogenesis.
Pituitary adenylate cyclase activating polypeptide (PACAP) signalling exerts
chondrogenesis promoting and protecting effects: implication
of calcineurin as a downstream target.
The 3D structure
of the pellet mimics embryonic development
of the limbs, and improves the intercellular communication essential for
chondrogenesis to occur [8, 9].