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. 2010 Mar;176(3):1390–1399. doi: 10.2353/ajpath.2010.090694

Figure 6.

Figure 6

The MEK1/2/ERK1/2 signaling cascade is activated in nerves of PMP22tg mice. Western blot analyses of peripheral nerve lysates from two-month-old (A–E) and of six-month-old (F) wild-type (wt) and PMP22tg mutant mice. The diagrams below the immunoblots illustrate the corresponding densitometric analyses of three experiments comprising two to five mice. JNK1 (A, 46 kDa) and IKBα (B, 37 kDa) do not show any increased phosphorylation in femoral quadriceps nerves in PMP22tg mice relative to wild-type. In contrast, stronger phosphorylation of ERK1/2 (pERK1/2, 44/42 kDa) is visible in femoral quadriceps (C) and sciatic nerves (D) of PMP22tg mice compared with wild-types. E: The upstream kinase of ERK1/2, MEK1/2 (45 kDa), is stronger phosphorylated in femoral quadriceps nerve of PMP22tg mice. F: The stronger ERK1/2-phosphorylation is still visible in femoral quadriceps nerves of six-month-old PMP22tg mice compared with wild-types. In all blots, staining with antibodies against the corresponding total protein serves as loading controls. G: Localization of phospho-ERK1/2 in single fiber preparations of two-month-old mice. In comparison with a more non-nuclear and faint labeling in PMP22wt (n = 3), femoral quadriceps nerves of PMP22tg mice (n = 3) reveal an additional phospho-ERK1/2 immunoreactivity (red, Cy3, arrow) in nuclei (DAPI, blue) of S100β-positive Schwann cells (green, FITC). Scale bar = 10 μm.