Abstract
Schwann cells play an important role in peripheral nerve function, and their dysfunction has been implicated in the pathogenesis of diabetic neuropathy and other demyelinating diseases. The physiological functions of insulin in Schwann cells remain unclear and therefore define the aim of this study. By using immortalized adult Fischer rat Schwann cells (IFRS1), we investigated the mechanism of the stimulating effects of insulin on the cell proliferation and expression of myelin proteins (myelin protein zero (MPZ) and myelin basic protein (MBP). The application of insulin to IFRS1 cells increased the proliferative activity and induced phosphorylation of Akt and ERK, but not P38-MAPK. The proliferative potential of insulin-stimulated IFRS1 was significantly suppressed by the addition of LY294002, a PI3 kinase inhibitor. The insulin-stimulated increase in MPZ expression was significantly suppressed by the addition of PD98059, a MEK inhibitor. Furthermore, insulin-increased MBP expression was significantly suppressed by the addition of LY294002. These findings suggest that both PI3-K/Akt and ERK/MEK pathways are involved in insulin-induced cell growth and upregulation of MPZ and MBP in IFRS1 Schwann cells.
Highlights
Diabetic peripheral neuropathy (DPN) is one of the complications of diabetes mellitus.It is reported to be caused by many factors, including abnormalities in polyol metabolic pathways, oxidative stress, and ion channel abnormalities, but the details of these causes remain unclear [1,2,3]. the etiology of DPN is clearly related to hyperglycemia, there are reports that insulin resistance exacerbates the pathogenesis of diabetic neuropathy in type 2 diabetes mellitus, and impaired insulin signaling in the peripheral nerves is thought to play a major role in the pathogenesis of diabetic neuropathy [4]
The etiology of DPN is clearly related to hyperglycemia, there are reports that insulin resistance exacerbates the pathogenesis of diabetic neuropathy in type 2 diabetes mellitus, and impaired insulin signaling in the peripheral nerves is thought to play a major role in the pathogenesis of diabetic neuropathy [4]
To examine whether IFRS1 has insulin receptors, we evaluated the expression of insulin receptor beta (IR-beta)
Summary
Diabetic peripheral neuropathy (DPN) is one of the complications of diabetes mellitus. The etiology of DPN is clearly related to hyperglycemia, there are reports that insulin resistance exacerbates the pathogenesis of diabetic neuropathy in type 2 diabetes mellitus, and impaired insulin signaling in the peripheral nerves is thought to play a major role in the pathogenesis of diabetic neuropathy [4]. Schwann cells, such as the expression of neurotrophic factors and myelin proteins and the myelination in co-culture with neuronal cells [20,21,22,23]. We investigated the mechanism by which insulin promotes the growth and expression of myelin component proteins in cultured Schwann cells using IFRS1
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
