Skip to main content
. Author manuscript; available in PMC: 2017 Jul 27.
Published in final edited form as: Kidney Int. 2016 Sep 22;91(1):86–95. doi: 10.1016/j.kint.2016.07.039

Figure 8. Effects of activin A on osteoclastogenesis.

Figure 8

Treatment of bone marrow mononuclear cells with RANK ligand (RANKL) for 4 days as described in Methods was used to induce differentiation to osteoclasts. Osteoclast production, which we have previously reported on,35 was marked by induction of the specific transcription factor nuclear factor of activated T cells c1 (NFATc1), and the osteoclast phenotype differentiation markers cathepsin K and integrin subunit β3. Treatment with activin A enhanced RANKL-stimulated osteoclastogenesis and induction of NFATc1, cathepsin K, and integrin β3. Activin A treatment did not affect levels of activin receptor type 2A (ActRIIA), and increased p-Smad2 associated with NFATc1, as shown in Figure 9. D, day; M-CSF, macrophage colony-stimulating factor.