| First Author | Zhang J | Year | 2022 |
| Journal | Oral Dis | Volume | 28 |
| Issue | 7 | Pages | 1958-1967 |
| PubMed ID | 33901321 | Mgi Jnum | J:350382 |
| Mgi Id | MGI:7660882 | Doi | 10.1111/odi.13888 |
| Citation | Zhang J, et al. (2022) Trim14 promotes osteoclastogenesis and noncanonical NF-kappaB activation by targeting p100/p52 in chronic periodontitis. Oral Dis 28(7):1958-1967 |
| abstractText | BACKGROUND: Periodontitis disease infection initiates host immune response, and alveolar bone damage is a hallmark of periodontitis. Bone damage occurs due to changes in osteoclast activity in response to local inflammation. Nuclear factor kappaB (NF-kappaB) signaling is essential for inflammatory responses and plays a pivotal role in osteoclast formation and activation. Tripartite motif 14 (Trim14) is a crucial regulator of the noncanonical NF-kappaB signaling. Here, we investigated the role of Trim14 in chronic periodontitis. METHODS: The development of immune cells and osteoclast formation was evaluated with flow cytometry, qRT-PCR, and histochemical staining. Proinflammatory cytokines were checked by ELISA and qRT-PCR. Protein expression was determined by immunoblotting. Also, the cemento-enamel junction-alveolar bone crest distance was evaluated in the mouse model. RESULTS: Development of innate and adaptive cells was not impaired from the deletion of Trim14. However, the genetic loss of Trim14 remarkably suppressed RANKL-induced osteoclastogenesis, without affecting TLR-induced proinflammatory cytokines except for Il-23a expression. The Trim14 deletion also suppressed the activation of noncanonical NF-kappaB signaling by targeting p100/p52. Importantly, the deletion of NIK diminished the effects of Trim14 on the inflammatory responses in vivo on chronic periodontitis responses. CONCLUSION: TRIM14 may be a positive regulator to promote osteoclastogenesis and proinflammatory cytokine secretion. |
