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[P3-2-15] Involvement of O-GlcNAcylation in dentin regeneration

〇Elina Pokharel¹, Tae-Young Kim¹, Anna Kim¹, Rana Bandana¹, Jae-Kwang Jung², Do-Yeon Kim⁴, Hitoshi Yamamoto⁵, Jung-Hong Ha⁶, Jae-Young Kim ¹, Chang-Hyeon An³ (1. Dept Biochem, Kyungpook Natl Univ Sch Dent , 2. Dept Oral Med, Kyungpook Natl Univ Sch Dent, 3. Dept Oral Maxillofac Radiol, Kyungpook Natl Univ Sch Dent, 4. Dept Pharmacol, Kyungpook Natl Univ Sch Dent, 5. Dept Histol Dev Biol, Tokyo Dent Coll, 6. Dept Conserv Dent, Kyungpook Natl Univ Sch Dent)

キーワード：OGA、Pulp cavity、Inflammation

O-GlcNAcylation is the posttranslational modification of the proteins catalyzed by two enzymes; OGT and OGA. O-GlcNAc modification of protein on serine or threonine residue is crucial for tissue specification, cell viability, and embryonic development. Moreover, the hyper O-GlcNAcylation of the cellular proteins has shown preventive effects during inflammation in various organs. However, its role during hard tissue formation, especially dentin formation and regeneration, has not been explored yet. In this study, the pharmacological elevation of O-GlcNAcylation by OGA inhibitor drug following up pulp expose in mouse molars resulted in reparative dentin formation via inflammation prevention. Altered morphological changes and cellular physiology were examined with histology and immunohistochemistry. OGA-inhibited specimens showed altered localization patterns of Nestin, NF-κB, MPO, Osteopontin, Runx2, TGF-β1, and TNF-∂ after 3 and 5 days from treatment. Furthermore, OGA inhibited specimens showed facilitated dentin-bridge formation after 42 days when compared with control. Micro-CT evaluation confirmed the facilitated dentin-bridge structure in the OGA-inhibited specimens. From these results, we concluded that hyper O-GlcNAcylation with OGA inhibition would facilitate reparative dentin formation via modulation of inflammation and signalling regulations.