| First Author | Geng YM | Year | 2019 |
| Journal | Mol Med Rep | Volume | 20 |
| Issue | 5 | Pages | 4193-4201 |
| PubMed ID | 31545469 | Mgi Jnum | J:298907 |
| Mgi Id | MGI:6453224 | Doi | 10.3892/mmr.2019.10688 |
| Citation | Geng YM, et al. (2019) LAPTM5 is transactivated by RUNX2 and involved in RANKL trafficking in osteoblastic cells. Mol Med Rep 20(5):4193-4201 |
| abstractText | The present study aimed to investigate the role of lysosomalassociated transmembrane protein 5 (LAPTM5) in osteoclast differentiation induced by osteoblasts. The results demonstrated that the expression levels of LAPTM5 were downregulated following runtrelated transcription factor 2 (RUNX2) silencing and upregulated following RUNX2 overexpression in ST2 cells. Chromatin immunoprecipitation analysis identified the binding of RUNX2 to the LAPTM5 promoter at the 1176 to 1171 position. Dualluciferase reporter assays confirmed that RUNX2 directly activated the LAPTM5 gene. The concentration of receptor activator of nuclear factorkappaB ligand (RANKL) protein in the cytoplasm and in the media was significantly increased following LAPTM5 knockdown. LAPTM5 silencing in ST2 cells enhanced osteoclastic differentiation of cocultured RAW264.7 cells. The present study indicated that expression of LAPTM5 was regulated by the interaction of RUNX2 with its promoter region and that LAPTM5 was involved in the trafficking of RANKL. These findings suggested a possible coupling mechanism between osteogenesis and osteoclastogenesis in which RUNX2 may be involved in osteoclast differentiation through the regulation of the lysosomeassociated genes that modulate RANKL expression. |
