Diabetic polyneuropathy (DPN) causes axonal injury and Schwann cells (SCs) might are crucial in this process. We investigated the direct interaction between SCs and dorsal root ganglion (DRG) neurons under hyperglycaemic condition and the effects of Schwann cell-conditioned media on neurite outgrowth of DRG neurons. We observed that high glucose impaired axonal growth in neuron-Schwann cells co-culture and in neuron monoculture exposed to the medium obtained from Schwann cells cultured in high glucose. We found that VEGF concentrations were significantly higher in Schwann cells-media under the high glucose condition than in those under control condition. The reduced neurite outgrowth observed in hyperglycaemic co-culture was inhibited by VEGF neutralizing antibody. Our results suggest that an increase of VEGF secretion by SCs under the diabetic condition would cause a defect of axonal regeneration, resulting in the development of diabetic neuropathy.
(2012). Schwann cells mediate the impairment of neurite growth by increased VEGF secretion in DRG neurons exposed to hyperglycemia. (Tesi di dottorato, Università degli Studi di Milano-Bicocca, 2012).
Schwann cells mediate the impairment of neurite growth by increased VEGF secretion in DRG neurons exposed to hyperglycemia
TAIANA, MICHELA MARIA
2012
Abstract
Diabetic polyneuropathy (DPN) causes axonal injury and Schwann cells (SCs) might are crucial in this process. We investigated the direct interaction between SCs and dorsal root ganglion (DRG) neurons under hyperglycaemic condition and the effects of Schwann cell-conditioned media on neurite outgrowth of DRG neurons. We observed that high glucose impaired axonal growth in neuron-Schwann cells co-culture and in neuron monoculture exposed to the medium obtained from Schwann cells cultured in high glucose. We found that VEGF concentrations were significantly higher in Schwann cells-media under the high glucose condition than in those under control condition. The reduced neurite outgrowth observed in hyperglycaemic co-culture was inhibited by VEGF neutralizing antibody. Our results suggest that an increase of VEGF secretion by SCs under the diabetic condition would cause a defect of axonal regeneration, resulting in the development of diabetic neuropathy.File | Dimensione | Formato | |
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