Injury-induced activation of ERK 1/2 in the sciatic nerve of healthy and diabetic rats

被引：14

作者：

Stenberg, Lena ^{[1
]}

Kanje, Martin ^{[2
]}

Martensson, Lisa ^{[2
]}

Dahlin, Lars B. ^{[1
]}

机构：

[1] Skane Univ Hosp, Dept Clin Sci Malmo Hand Surg, SE-20502 Malmo, Sweden

[2] Lund Univ, Dept Biol, Lund, Sweden

来源：

NEUROREPORT | 2011年 / 22卷 / 02期

基金：

瑞典研究理事会;

关键词：

BioBreeding rats; diabetes; nerve injury; nerve transection; neuropathy; streptozotocin; phosphorylation of extracellular-signal regulated kinase 1/2; SIGNALING PATHWAY; PERIPHERAL-NERVE; SENSORY NEURONS; PROTEIN-KINASES; SCHWANN-CELLS; NEUROPATHY; PHOSPHORYLATION; NEUROTROPHIN-3; REGENERATION; MYELINATION;

D O I：

10.1097/WNR.0b013e328342986c

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Phosphorylation of extracellular-signal-regulated kinase 1/2 (p-ERK 1/2) was investigated by immunohistochemistry at 30 min, 1 h, and 48 h after nerve transection in the sciatic nerve of healthy and diabetic [ streptozotocin (STZ)-induced diabetes mellitus and BioBreeding (BB; i.e. DR. lyp/lyp or BBDP)] rats. Transection injury increased the intensity of p-ERK 1/2 in nerve stumps at all time points. Staining was confined to Schwann cells with occasional faint staining in single axons. In diabetic rats, a lower intensity of p-ERK 1/2 was found at 1 and 48 h in the distal and proximal nerve stumps compared with healthy rats. STZ-induced diabetic rats were not different from BB rats. p-ERK 1/2 is activated differentially in Schwann cells after nerve injury in diabetic rats, whereas activation in STZ-induced diabetic rats did not differ from BB rats. NeuroReport 22: 73-77 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

引用

页码：73 / 77

页数：5

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