STC1 and especially STC2 are two potent targets for inhibition during development enhancing height growth. So I open it up to brainstorming to try to find inhibitors.
Stanniocalcin 1 Acts as a Paracrine Regulator of Growth Plate Chondrogenesis
"During embryogenesis, the expression of mammalian stanniocalcin (STC1) in the appendicular skeleton suggests its involvement in the regulation of longitudinal bone growth. Such a role is further supported by the presence of dwarfism in mice overexpressing STC1. Yet, the STC 1 inhibitory effect on growth may be related to both postnatal metabolic abnormalities and prenatal defective bone formation. In our study, we used an organ culture system to evaluate the effects of STC on growth plate chondrogenesis, which is the primary determinant of longitudinal bone growth. Fetal rat metatarsal bones were cultured in the presence of recombinant human STC (rhSTC). After 3 days, rhSTC suppressed metatarsal growth, growth plate chondrocyte proliferation and hypertrophy/differentiation, and extracellular matrix synthesis. In addition, rhSTC increased the number of apoptotic chondrocytes in the growth plate. In cultured chondrocytes, rhSTC increased phosphate uptake, reduced chondrocyte proliferation and matrix synthesis, and induced apoptosis. All these effects were reversed by culturing chondrocytes with rhSTC and phosphonoformic acid, an inhibitor of phosphate transport. The rhSTC-mediated inhibition of metatarsal growth and growth plate chondrocyte proliferation and hypertrophy/differentiation was abolished by culturing metatarsals with rhSTC and phosphonoformic acid. STC1 inhibits longitudinal bone growth directly at the growth plate. Such growth inhibition, likely mediated by an increased chondrocyte phosphate uptake, results from suppressed chondrocyte proliferation, hypertrophy/differentiation, and matrix synthesis and by increased apoptosis. Last, the expression of both STC1 and its binding site in the growth plate would support an autocrine/paracrine role for this growth factor in the regulation of growth plate chondrogenesis. "
"sodium-dependent Pi (NaPi) transporter(s) may be a target of STC1 activity"
PFA is an additional inhibitor of phosphate transport also used in the study. STC decreased the hypertrophic or proliferatize zone height to an additional degree than PFA which had a relatively minor decrease. STC also decreased cartilage matrix synthesis to a much greater degree than PFA.
"100 ng/ml rhSTC significantly increased Pit-1 mRNA expression in the metatarsal growth plate, whereas it decreased mRNA expression of FGF23"<-FGF23 is involved in phosphate homeostasis and increases chondrocyte hypertrophy.
"When compared with control mice, STC transgenic mice exhibited a 30-50% postnatal growth reduction."
"In a study on ADTC5 cells (a chondrogenic cell line), treatment with Pi and Ca2+ led to a decrease in the Bcl-2/Bax ratio, which is believed to disrupt the mitochondrial membrane and promote release of mitochondrial components, irreversibly engaging the cell toward apoptosis"
STC1 overexpression enhances osteoblast differentiation according to Stanniocalcin 1 stimulates osteoblast differentiation in rat calvaria cell cultures.
The murine stanniocalcin 1 gene is not essential for growth and development.
"Stc1 function is not essential for growth or reproduction in the mouse."
STC1 null mice had improved bone density but does that mean increased height? Weight growth was lower in STC1 null mice but no measurements of longitudinal bone growth were provided but they did say that growth was normal.
STC2 deletion however does increase growth according to The murine stanniocalcin 2 gene is a negative regulator of postnatal growth.
More on STC1 and STC2: Human stanniocalcin-2 exhibits potent growth-suppressive properties in transgenic mice independently of growth hormone and IGFs.