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Enteric glial cell activation protects enteric neurons from damage due to diabetes in part via the promotion of neurotrophic factor release
Author(s) -
Luo P.,
Liu D.,
Li C.,
He W.X.,
Zhang C.L.,
Chang M.J.
Publication year - 2018
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.13368
Subject(s) - glial cell line derived neurotrophic factor , enteric nervous system , glial fibrillary acidic protein , neurotrophic factors , endocrinology , medicine , nerve growth factor , streptozotocin , neurotrophin 3 , neurotrophin , diabetes mellitus , leptin , neuroglia , ileum , brain derived neurotrophic factor , immunohistochemistry , biology , central nervous system , receptor , obesity
Abstract Background Diabetes can result in pathological changes to enteric nervous system. Our aim was to test the dynamic changes of enteric neurons and identify the role of enteric glial cells ( EGC s) in regulating enteric neuron expression in diabetic rats. Methods A single injection of streptozotocin ( STZ ) was used to establish diabetic rats. Animals were randomly distributed into diabetic 1‐, 4‐, 8‐, and 16‐week groups, as well as age‐matched control groups. The PGP 9.5‐ and glial fibrillary acidic protein (GFAP)‐immunopositive cells were quantified by immunohistochemistry. The protein levels of PGP 9.5, Ch AT , nNOS , S‐100β, and c‐fos were determined by western blotting. The levels of nerve growth factor (NGF), neurotrophin 3 (NT‐3), and glial cell‐derived neurotrophic factor (GDNF) were tested by ELISA . Key Results An increase in blood glucose and a decrease in body weight were observed following STZ administration. PGP 9.5 expression did not change in the diabetic ileum. However, Ch AT increased after 16 weeks, and nNOS decreased after 8 and 16 weeks in the ilea of diabetic rats. The absence of degeneration of enteric neurons during the acute stage of the disease could be the consequence of the up‐regulation of GFAP , S‐100β, and c‐fos. Moreover, the content of NGF , NT ‐3, and GDNF in the ileum increased by varying degrees after 1 and/or 4 weeks of diabetes. Using 2 co‐culture models of EGC s and SH ‐ SY 5Y cells in a high glucose condition, the supportive role of EGC s was further confirmed. Conclusions & Inferences Enteric glial cell activation can protect enteric neurons from damage due to diabetes in the acute stage of the disease, in part via the promotion of neurotrophin release.