Bystin as a novel marker for reactive astrocytes in the adult rat brain following injury

• Published in: The European journal of neuroscience Vol. 20; no. 4; pp. 873 - 884
• Main Authors: Sheng, Jiansong, Yang, Shuo, Xu, Lei, Wu, Chunhua, Wu, Xuefei, Li, Aiqun, Yu, Yi, Ni, Hengjian, Fukuda, Michiko, Zhou, Jiawei
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.08.2004
• Subjects: Animals; Astrocytes - chemistry; Astrocytes - metabolism; Astrocytes - pathology; Biomarkers - analysis; Brain Injuries - chemically induced; Brain Injuries - metabolism; Brain Injuries - pathology; Cell Adhesion Molecules - analysis; Cell Adhesion Molecules - biosynthesis; Cell Adhesion Molecules - genetics; Cell Differentiation; Cells, Cultured; Cerebral Cortex - chemistry; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Cloning, Molecular; cytokine; Female; inflammation; Molecular Sequence Data; Oxidopamine; Pregnancy; rat; Rats; Rats, Sprague-Dawley; reactive astrocytes; substantia nigra
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1111/j.1460-9568.2004.03567.x

Bystin has been identified as a protein which mediates cellular interactions between trophoblastic and endometrial epithelial cells by forming complexes with two partners, trophinin and tastin, during embryo implantation. However, the presence of bystin in the central nervous system has not been demonstrated. Here, we report the cloning of the full‐length cDNA of the rat bystin gene from adult brain. Immunohistochemical and RT‐PCR analysis showed that the levels of bystin expression were markedly up‐regulated in the both 6‐hydrodopamine‐lesioned rat nigrostriatum and stab‐lesioned cerebral cortex in adult rats. Double immunofluorescence staining revealed that most bystin‐expressing glial cells were astrocytes (immature or mature). To determine the mechanisms for the up‐regulation of bystin expression in glial cells, primary cultures of postnatal cortical astrocytes were employed. Western blot analysis showed that the expression of bystin was elevated by treatment with pro‐inflammatory mediators lipopolysaccharide and interleukin‐1β. Nerve growth factor known to be released after brain injury also induced bystin expression in the cultures. Exposure of astrocyte cultures to the differentiating agent forskolin resulted in up‐regulation of bystin followed by a pronounced astrocytic stellation. The results suggest that the injury in the adult brain induces spatiotemporal up‐regulation of bystin and it could be influenced, at least in part, by elevation of intracellular cAMP level. Bystin expressed by reactive astrocytes may be involved in their differentiation during the inflammatory processes following brain injury. The reappearance of bystin may also indicate that some reactive astrocytes have the capacity to recapitulate early developmental stages.