FIGURE 1.
Clinical course of MOG35‐55‐induced EAE in Fgfr2ind−/− mice. Oligodendroglial FGFR2 deletion was achieved in 4–5‐week‐old female Plpcre +:Fgfr2flox / flox mice by daily injections of tamoxifen over five consecutive days. EAE was induced in 12–13‐week‐old mice using the MOG35‐55 peptide. EAE symptoms were investigated until day 60 p.i. Spinal cord tissues were collected in the acute (day 18–20 p.i.) and the chronic phase of EAE (day 60 p.i.). (A) Confirmation of FGFR lox and cre expression in mutant mice by PCR and agarose gel electrophoresis. (B) The onset of symptoms was not different between Fgfr2ind −/− mice and controls. The peak of symptoms was on day 15 p.i. in Fgfr2ind −/− mice and on day 14 p.i. in controls. From day 24 onwards Fgfr2ind −/− mice had a mild paraparesis, whereas controls still had a severe paraparesis (n = 14 in Fgfr2ind −/− mice and n = 13 in control). FGF/FGFR expression in the spinal cord in the acute and chronic phase of MOG35 ‐ 55‐induced EAE. (C) FGFR2 protein expression was less in Fgfr2ind −/− mice in the acute phase of EAE. FGFR1, FGF2 and FGF9 were not regulated in the acute phase of EAE. (D) FGFR2, FGF2 and FGF9 protein expression was reduced in Fgfr2ind −/− mice in the chronic phase of EAE. FGFR1 expression was not regulated in the chronic phase. Representative western blot images and the quantification are shown. Data are presented as mean ±SEM. *p < 0.05, **p < 0.005.