Slc26a2 is involved in sulfur intake by chondrocytes and mutations in Slc26a2 can cause Diastrophic Dysplasia, which causes chondrocyte undersulfation and reduces height.  Read more about DTD here.  A supplement that upregulates Slc26a2 expression could be an alternative to increasing IGF-1 expression and given that DTD is a disease treatments will be developed that may be applicable to people with operating normal growth plates to grow taller.

Multiple Roles of the SO42-/Cl-/OH- exchanger Slc26a2 in Chondrocyte functions.

“Mutations in the SO42-/Cl-/OH- exchanger Slc26a2 cause the disease diastrophic dysplasia (DTD), resulting in aberrant bone development and therefore skeletal deformities. DTD is commonly attributed to a lack of chondrocyte SO42- uptake and proteoglycan sulfation. However, the skeletal phenotype of patients with DTD is typified by reduction in cartilage and osteoporosis of the long bones. Chondrocytes of patients with DTD are irregular in size and have a reduced capacity for proliferation and terminal differentiation. This raises the possibility of additional roles for Slc26a2 in chondrocyte function. Here, we examined the roles of Slc26a2 in chondrocyte biology using two distinct systems: mouse progenitor mesenchymal cells differentiated to chondrocytes and freshly isolated mouse articular chondrocytes differentiated into hypertrophic chondrocytes. Slc26a2 expression was manipulated acutely by delivery of Slc26a2 or shSlc26a2 with lentiviral vectors. Slc26a2 is essential for chondrocyte proliferation and differentiation, and for proteoglycan synthesis. Slc26a2 also regulates the terminal stage of chondrocyte cell size expansion{thus perhaps extra Slc26a2 could increase height}.”

“Slc26a2 functions as a SO42-/Cl-/OH exchanger that is exquisitely regulated by extracellular Cl-”

“Slc26a2 expression is highly enriched in the long bone proliferating zone.”  Slc26a2 is minimally expressed in the resting zone but moderately expressed in the hypertrophic zone.  Thus, perhaps Slc26a2 plays a role in chondrocyte differentiation.

“Proteoglycan sulfation depends on SO42- uptake by chondrocytes. The SO42- transporter Slc26a2 mediates most SO42- uptake by chondrocytes”

IGF-1 activates Slc26a2.

“Knockdown of Slc26a2 strongly inhibited the effect of IGF-1 on proteoglycan synthesis, and IGF-1 had a very modest effect on proteoglycan synthesis in cells overexpressing Slc26a2.  Inhibition of PI3K by LY294002 inhibited the effects of both Slc26a2 and IGF-1.”<-Thus Slc26a2 is highly responsible for the rate of proteoglycan synthesis.  High IGF-1 can make up for a Slc26a2 deficit and vice versa.

“treatment with IGF-1 and overexpression of Slc26a2 increased proteoglycan synthesis, whereas knockdown of Slc26a2 inhibited synthesis.”

“IGF-1 and Slc26a2 increased chondrocyte size, with a combined effect smaller than the additive effect. PI3K activity was necessary for both IGF-1 mediated and Slc26a2 mediated chondrocyte volume expansion.”

“the function of Slc26a2 in chondrocytes cannot be compensated for by any of the other SLC26 SO42- transporters”

“Slc26a2 is constitutively phosphorylated by PI3K”