Hyperglycemia Increases Mitochondrial Protein Expression in the Absence of Oxidative Stress

Abstract

Long-term diabetes may cause diabetic peripheral neuropathy (DPN). Hyperglycemic-induced oxidative stress is widely accepted as the contributing factor in the development of diabetic complications. The mitochondrion has been singled out as the site of increased production of superoxide (O2-). Oxidative stress has been shown to be particularly deleterious to mitochondria because it is intimately associated with apoptosis. We utilized proteomics to study the effect chronic hyperglycemia may have on enriched Schwann Cell (SC) mitochondria. Through stable isotope labeling of amino acids in cell culture (SILAC) and mass spectrometry we were able to determine that chronic hyperglycemia induced an overexpression of proteins important in detoxification that occurred independently from oxidative stress. We conclude that the SCs under hyperglycemic stress react by increasing the levels of protective proteins to counter the influx of high glucose thus affording protection not only for itself but the crucial axon it enwraps.