“we investigated whether C/EBPβ represses type II collagen (COL2A1) expression and is involved in the regulation of sex-determining region Y-type high mobility group box 9 (SOX9), a crucial factor for transactivation of Col2a1. Endogenous expression of C/EBPβ in the embryonic growth plate and differentiated ATDC5 cells were opposite to those of COL2A1 and SOX9. Overexpression of C/EBPβ by adenovirus vector in ATDC5 cells caused marked repression of Col2a1. The expression of Sox9 mRNA and nuclear protein was also repressed, resulting in decreased binding of SOX9 to the Col2a1 enhancer. Knockdown of C/EBPβ by lentivirus expressing shRNA caused significant stimulation of these genes in ATDC5 cells. Reporter assays demonstrated that C/EBPβ repressed transcriptional activity of Col2a1. Deletion and mutation analysis showed that the C/EBPβ core responsive element was located between +2144 and +2152 bp within the Col2a1 enhancer. EMSA and ChIP assays also revealed that C/EBPβ directly bound to this region. Ex vivo organ cultures of mouse limbs transfected with C/EBPβ showed that the expression of COL2A1 and SOX9 were reduced upon ectopic C/EBPβ expression. Together, these results indicated that C/EBPβ represses the transcriptional activity of Col2a1 both directly, and indirectly through modulation of Sox9 expression. This consequently promotes the phenotypic conversion from proliferative to hypertrophic chondrocytes during chondrocyte differentiation.”
So maybe knockdown of CEBP-Beta could increase height? It upregulates chondrogenic genes but we’d have to see the effects on the growth plate to be sure.
“The expression of COL10A1, RUNX2, and MMP13 was misexpressed through the tibias that were transfected with C/EBPβ, compared with LacZ control. Forced expression of C/EBPβ may lead the ectopic expression of these genes even in the regions that do not show the morphological hypertrophy because C/EBPβ is reported as a direct regulator of them. Moreover, the expression of SOX9 was also decreased and restricted to a small upper area of the growth plate by overexpression of C/EBPβ, similar to the expression of COL2A1. Together, these results further confirmed that C/EBPβ could be involved in regulation of phenotypic conversion from proliferative to hypertrophic chondrocytes by repressing the genes characteristic of proliferative chondrocytes during chondrocyte differentiation.”