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. 2018 May;1864(5Part A):1609–1621. doi: 10.1016/j.bbadis.2018.01.028

Fig. 1.

Fig. 1

Vps33b and Vipar deficient mice develop dry skin with a defective water loss barrier that is characterised by hyperplasia and hyperproliferation. A - Control, Vps33bfl/flERT2 and Vipas39fl/flERT2 keratinocyte lysates blotted for VPS33B, VIPAR and GAPDH expression, arrows indicate VPS33B and VIPAR specific bands. B - Photos of dorsal skin of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 mice. Vps33bfl/flERT2 photo reproduced from [5]. C - Trans-epidermal water loss (TEWL) of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 mice. D - H&E staining of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 skin with increased purple granular staining, spongiosis (double arrows) and thicker SC (single arrow). E - Epidermal thickness of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 mice, the distance from the dermal-epidermal junction to the SG-SC junction. F - The number of nuclei in the epidermis of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 mice. G - Average keratinocyte size of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 mice: epidermal area divided by number of nuclei. H - Representative Ki67 staining of control, Vps33bfl/flERT2 and Vipas39fl/flERT2 skin sections, counterstained with DAPI. I - Quantification of the number of Ki67 stained nuclei per mm of epidermis. Western blots are representative of two independent western blotting experiments. Scale bars = 50 μm. Immunofluorescent images are a maximum projection of a z-stack. For epidermal measurements three fields of view were measured per mouse, the number of independent murine samples mice analysed (n) are indicated on the graphs. * p ≤ 0.05, ** p ≤ 0.01, **** p ≤ 0.0001.