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. Author manuscript; available in PMC: 2021 Oct 5.
Published in final edited form as: Glia. 2020 Aug 3;69(1):91–108. doi: 10.1002/glia.23886

FIGURE 6.

FIGURE 6

Schwann cells (SCs) lacking integrin αV proliferate and respond to TFGβ1 normally. (a,b,d,e) Longitudinal sections of Itgavf/f and Itgavf/f; P0-Cre sciatic nerves were immunostained for proliferation markers Ki67 (green) at P3 (a,b) and PH3 (green) at P5 (d,e). Both were costained with neurofilament (NF) (red) and DAPI (blue). (c,f) No appreciable difference in the percentage of Ki67-positive cells (student’s t test, n = 4 nerves) or of PH3-positive cells (student’s t test, n = 3 animals/genotype, SEM error bars) was detected between Itgavf/f and Itgavf/f; P0-Cre. (g–r) SMAD4 was properly shuttled to the nucleus in αV mutant cells. SCs isolated from Itgavf/f or Itgavf/f; P0-Cre sciatic nerves were cultured, treated with TGFβ1, then immunostained for SOX10 (to identify SCs), SMAD4, and DAPI. SMAD4 localized more in the cytoplasm of untreated cells (m–r), but when treated with TFGβ1, SMAD4 localized more in the nucleus of both Itgavf/f and Itgavf/f; P0-Cre SCs (g–l). Scale bar for (g-r) is 30 μm. (s) Average %nuclear-SMAD4/Sox10-positive cells were comparable between Itgavf/f and Itgavf/f; P0-Cre (student’s t test, n = 5 animals/genotype, ≥1,370 Sox10-positive cells quantified per genotype, SEM error bars). Mean %Sox10-positive cells: Itgavf/f 51%, Itgavf/f; P0-Cre 67%