Anti-MEF2C polyclonal antibody

Activation of osteoclast formation and function is crucial for the development of osteolytic diseases such as osteoporosis. RANKL (receptor activator of nuclear factor-kappa B ligand) activates NF-kappa B (nuclear factor kappa B), MAPK (mitogen-activated protein kinase), and NFATc1 (nuclear factor of activated T-cells, cytoplasmic 1) signaling pathways to induce osteoclastogenesis. In this study, we demonstrated that SB239063, a p38-specific inhibitor, suppressed osteoclastogenesis and bone resorption via inhibiting phosphorylation of MEF2C (myocyte enhancer factor 2C) and subsequently leading to MEF2C degradation by ubiquitination. Knockdown of MEF2C impaired osteoclast formation due to decreased c-Fos expression. Furthermore, MEF2C can directly bind to the promoter region of c-Fos to initiate its transcription. Interestingly, overexpression of either MEF2C or c-Fos can partially rescue the inhibitory effect of SB239063 on osteoclastogenesis. In addition, in vivo data proved that SB239063 also played a preventive role in both LPS (lipopolysaccharide)-and OVX (ovariectomy)-induced bone loss in mice. In conclusion, our results show that SB239063 can be a potential therapy for osteolytic diseases, and a novel p38/MEF2C/c-Fos axis is essential for osteoclastogenesis.

We report a case of microsecretory adenocarcinoma of the hard palate. The patient is a 37-year-old woman with a 15 mm submucosal tumor, which was incidentally found by her primary care dentist, in her hard palate. Preoperative magnetic resonance imaging revealed a tumor exhibiting high signal on T2-weighted image, which was gradually enhanced on dynamic study. Histologically, the tumor border was ill-defined without fibrous capsule and adjoined minor salivary gland with permeative infiltration at the tumor periphery. The tumor comprised intercalated duct-like cells with polygonal narrow eosinophilic to clear cytoplasm and small, uniform oval nuclei. These cells formed small infiltrative microcysts, tubules and fascicular cords collecting pale basophilic secretions and small vacuoles setting in an abundant fibromyxoid stroma. The tumor cells were positive for CK AE1+AE3, S-100 protein, and p63, while are completely negative for p40, alpha-SMA, and calponin. TheMEF2C-SS18fusion was identified by reverse transcriptase-polymerase chain reaction followed by Sanger sequencing. The combination of characteristic histology, immunophenotype, and presence ofMEF2C-SS18fusion indicated the diagnosis of microsecretory adenocarcinoma of the hard palate, an entity described only recently. Post-operative course was uneventful and there was no evidence of disease at 4 months after surgery.