Roles of senescence marker protein 30 on the nervous system

• 발행기관: 한국노년학회
• 저자명: Jaewon Lee
• 간행물 정보: 『한국노년학회 학술대회 논문집』2017년 한국노인과학학술대회, 247~247쪽, 전체 1쪽
• 주제분류: 사회과학 > 사회복지학
• 파일형태: PDF
• 발행일자: 2017.11.03

영문 초록

The physiological function of SMP30 has not been understood for more than a decade after its discovery, despite evidence that the amount of SMP30 has decreased in the aging process. In addition, the functional roles of SMP30 in the brain have not been investigated in aging and neurodegenerative diseases. Although the antioxidant property of SMP30 has been proposed to be mediated by its gluconolactonase (GNL) function, pathological impacts of SMP30 deficiency independent of VC biosynthesis have not been studied in neurodegenerative diseases. We have evaluated the effect of SMP30 deficiency on Parkinson s disease (PD) model. Wild-type (WT) and SMP30 KO mice supplemented with VC were treated with MPTP. Our results showed that MPTP-induced dopaminergic neuronal loss and the motor function impairment were more significant in the SMP30 KO mice. Reactive oxygen species generation and microglia activation were higher in MPTP-treated SMP30 KO mice. However, SMP30 deficiency attenuated MPTP-induced astrocyte activation and glia-derived neurotrophic factor production. Cultures of astrocyte derived from WT and SMP30 KO mice revealed that SMP30 deficiency abolished MPP+-induced astroglial activation by blocking the ERK pathway. Taken together, our findings demonstrate that SMP30 deficiency increases the severity of PD and suggest a beneficial role of SMP30 in protective astrocyte activation in response to neurodegeneration.

키워드

Glial activation Oxidative stress Parkinson s disease Senescence marker protein 30