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Glial cell line‐derived neurotrophic factor is expressed by inflammatory cells in the sciatic nerves of Lewis rats with experimental autoimmune neuritis
Author(s) -
Ahn Meejung,
Jin JaeKwang,
Moon Changjong,
Matsumoto Yoh,
Koh ChangSung,
Shin Taekyun
Publication year - 2010
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/j.1529-8027.2010.00258.x
Subject(s) - glial cell line derived neurotrophic factor , neurotrophic factors , neuritis , medicine , sciatic nerve , neuroprotection , inflammation , pathogenesis , immunohistochemistry , endocrinology , pathology , immunology , surgery , receptor
Neurotrophic factors, including glial cell line‐derived neurotrophic factor (GDNF), have been known to play a role in neuroprotection in the injured peripheral nervous system (PNS). To evaluate the involvement of GDNF in experimental autoimmune neuritis (EAN) pathogenesis, the expression of GDNF in rat sciatic nerves with EAN was studied. Western blot analysis showed that the level of GDNF protein significantly increased 1.8‐fold at the paralytic stage of EAN at day 12 post‐immunization (PI) (p < 0.01), and its level further increased approximately 2.5‐fold at day 21 PI (p < 0.001) in the sciatic nerves of EAN‐affected rats compared with those of control rats, and then declined thereafter at day 28 PI. Immunohistochemical analysis showed that axons and Schwann cells constitutively contained GDNF in normal controls. In sciatic nerves with EAN at day 12 PI, GDNF was immunostained in infiltrating inflammatory cells including macrophages and T cells. Collectively, we postulate that GDNF plays a regulatory role in EAN paralysis. A paradoxical role of inflammatory cells to ameliorate PNS inflammation remains to be further studied in EAN, an animal model of human demyelinating disease.