Skip to main content
. Author manuscript; available in PMC: 2020 May 1.
Published in final edited form as: J Tissue Eng Regen Med. 2019 Apr 15;13(5):823–834. doi: 10.1002/term.2834

Figure 5. Mechanisms induced by MC-GAG on osteoprogenitors and osteoclast progenitors.

Figure 5.

MC-GAG induces osteogenic differentiation of primary hMSCs via an autogenous activation of the canonical BMPR signaling pathway with phosphorylation of Smad1/5/8 (Mechanism 1, green arrow). MC-GAG directly inhibits viability, proliferation, and resorptive activity of osteoclasts even in the absence of differentiating hMSCs (Mechanism 2A, red lines). MC-GAG also upregulates OPG expression through an ERK1/2 dependent pathway, correlating to an indirect inhibition of resorptive activity but not viability or proliferation in co-culture with differentiating hMSCs (Mechanism 2B, red arrows and lines).