Noggin expression maintains cranial suture patency

We are using murine models to study the mechanisms governing cranial suture biology In these models, the posterior frontal (PF) suture fuses while all other sutures, including the sagittal (SAG) and coronal (COR) remain patent. Using these models, our laboratory and others have localized the expression of osteoinductive cytokines, such as TGF-beta1 and FGF-2, to the dura mater underlying the fusing PF suture.(1-3) In addition, we have shown low-level expression of these same cytokines in the patent SAG and COR dura mater. Previously, we had suspected that SAG and COR suture patency was simply the result of inadequate levels of osteoinductive cytokines; however, recent data from our laboratory suggests the SAG and COR dura mater may actively maintain overlying suture patency by providing an osteogenic antagonist called Noggin. Furthermore, the PF suture may, in part, fuse by actively suppressing Noggin expression. Noggin is a secreted glycoprotein that naturally antagonizes the osteogenic effects of BMPs. Noggin inactivates BMPs by preventing them from binding to their cognate receptor, thereby effectively reducing their extracellular morphogenetic gradients and preventing bone formation.