Articles

  • the Korean Society for Brain and Neural Sciences

Article

Original Article

Exp Neurobiol 2015; 24(2): 133-138

Published online June 30, 2015

https://doi.org/10.5607/en.2015.24.2.133

© The Korean Society for Brain and Neural Sciences

Growth Differentiation Factor 15 Expression in Astrocytes After Excitotoxic Lesion in the Mouse Hippocampus

Min-Hee Yi1, Enji Zhang1, Hyunjung Baek1,2, Sena Kim1,4, Nara Shin1,3, Joon Won Kang2, Sunyeul Lee3, Sang-Ha Oh4 and Dong Woon Kim1*

1Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon 301-747, Departments of 2Pediatrics, 3Anesthesia and Pain Medicine, 4Plastic Surgery, Chungnam National University Hospital, Daejeon 301-721, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-42-580-8207, FAX: 82-42-586-4800
e-mail: visnu528@cnu.ac.kr

Received: February 3, 2015; Revised: February 16, 2015; Accepted: February 21, 2015

Abstract

Growth differentiation factor 15 (GDF15) is, a member of the transforming growth factor β (TGF-β) superfamily of proteins. Although GDF15 is well established as a potent neurotrophic factor for neurons, little is known about its role in glial cells under neuropathological conditions. We monitored GDF15 expression in astrocyte activation after a kainic acid (KA)-induced neurodegeneration in the ICR mice hippocampus. In control, GDF15 immunoreactivity (IR) was evident in the neuronal layer of the hippocampus; however, GDF15 expression had increased in activated astrocytes throughout the hippocampal region at day 3 after the treatment with KA. LPS treatment in astrocytes dramatically increased GDF15 expression in primary astrocytes. In addition, LPS treatment resulted in the decrease of the IκB-α degradation and increase of the phosphorylation level of RelA/p65. These results indicate that GDF15 has a potential link to NF-κB activation, making GDF15 a valuable target for modulating inflammatory conditions.

Keywords: GDF15, Astrocyte, Excitotoxicity, NF kappaB signaling