Oral

[O2-E-PM2-04] Effects of microphthalmia-associated transcription factor on remodeling in masseter muscle

〇Megumi Nariyama¹, Yoshiki Ohnuki², Kenji Suita², Misao Ishikawa³, Aiko Ito⁴, Ichiro Matsuo⁵, Yoshio Hayakawa⁶, Yoshinobu Asada¹, Satoshi Okumura² (1. Dept Pediatr Dent, Tsurumi Univ Sch Dent Med, 2. Dept Physiol, Tsurumi Univ Sch Dent Med, 3. Dept Oral Anat, Tsurumi Univ Sch Dent Med, 4. Dept Orthodont, Tsurumi Univ Sch Dent Med, 5. Dept Periodont, Tsurumi Univ Sch Dent Med, 6. Dept Dent Anesthesiol, Tsurumi Univ Sch Dent Med)

Keywords:mitf遺伝子、咬筋、組織リモデリング

It has been reported that microphthalmia-associated transcription factor (MITF) plays an important role for the development of cardiac remodeling in response to chronic catecholamine stress. However, the role of MITF in masseter muscle (MA) remains poorly understood. To clarify the role of MITF on MA, we examined the effects of mitf mutation on muscle fibrosis, myocyte apoptosis, myocyte oxidative DNA damage, and signal transduction in mice with mitf gene mutation (mi/mi). Muscle atrophy, fibrosis area and myocyte apoptosis in MA were much greater in mi/mi, compared to the WT. Phosphorylation of Akt and mTOR, which are known as negative regulator of autophagy, was significantly increased, but p62 phosphorylation, an accelerator of autophagy, was significantly decreased in mi/mi than in WT. In addition, expressions of p62 and LC3 were significantly greater in mi/mi than in WT. The number of 8-OHdG (8-hydroxy-2’-deoxyguanosine) positive cells was significantly increased in mi/mi than in WT. Expressions of Nox2 and oxidized proteins were significantly greater in mi/mi than in WT. Survival rate was reduced in mi/mi than in WT. These results suggest that MA remodeling in mi/mi might be mediated through the oxidative stress with the decreased autophagic activity.