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Schwann cell is a target in ischemia–reperfusion injury to peripheral nerve
Author(s) -
Iida Haruyasu,
Schmeichel Ann M.,
Wang Yanping,
Schmelzer James D.,
Low Phillip A.
Publication year - 2004
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20159
Subject(s) - tunel assay , axon , reperfusion injury , schwann cell , terminal deoxynucleotidyl transferase , apoptosis , ischemia , nerve fiber , peripheral nerve injury , oxidative stress , immunohistochemistry , medicine , nerve injury , hindlimb , pathology , biology , endocrinology , anatomy , anesthesia , sciatic nerve , biochemistry
Ischemia–reperfusion (IR) causes oxidative injury and ischemic fiber degeneration due to injury of the neuron and axon. In this study, we explore the effect of oxidative stress on Schwann cells, as a specific peripheral nerve target, using our established rat model for IR injury. Fifty‐six rats were used. Six groups ( N = 8 each) underwent complete hindlimb ischemia for 4 h, followed by reperfusion durations of 0 h, 3 h, 7 days, 14 days, 28 days, and 42 days. One group underwent sham operation ( N = 8). We evaluated immunohistochemical labeling for oxidative injury using anti‐8‐hydroxydeoxyguanosine (8‐OHdG). To identify cells committed to apoptosis, we studied immunolabeling to caspase‐3 and terminal deoxynucleotidyl transferase (TdT)‐mediated dUTP‐biotin nick end labeling (TUNEL) positivity. Only minimal positivity was seen in the sham, 0‐h, and 3‐h groups. Positivity to 8‐OHdG, caspase‐3, and TUNEL increased significantly in groups undergoing longer reperfusion (8‐OHdG, 7–28 days; caspase‐3, 14–42 days; TUNEL, 14–42 days). The positive cells surrounding axons were identified as being Schwann cells by their configuration and colabeling with S‐100. We conclude that apoptosis of Schwann cells occurs during reperfusion and continues even when axons regenerate. Schwann cell apoptosis could contribute to impairment of axonal function and efficiency of fiber regeneration. Both these abnormalities are known to occur in experimental and human diabetic nerves. Muscle Nerve, 2004