For epidermal protein, mouse skin samples were placed on an ice-cold glass plate, and the epidermis was removed with a razor blade and placed into RIPA buffer containing 1% Triton X-100, protease inhibitor cocktail (Sigma-Aldrich Co., Saint Louis, MO), and phosphatase inhibitor cocktail I, II (Sigma-Aldrich Co).
Collagen density in mouse skin samples was examined by picrosirius red staining, and multiphoton microscopy.
Formalin-fixed, paraffin-embedded mouse skin samples were processed and stained according to routine Haematoxylin and Eosin (H&E) protocol.
Mast cells were visualized and quantified in mouse skin samples using toluidine blue (TBO) staining (pH = 2).
To analyze miR-203 expression in injured skin, in situ hybridizations were performed on sections of mouse skin samples collected at 3 and 5 days post wounding.
Interestingly, a very different situation applied to mouse skin samples, in which IL-1F8 levels were very high and further increased with inflammation.
To examine the status of hair germ between control and Pofut1/Tgfb3-Cre mice, back skin samples at P22 (telogen) and P24 (early anagen) were analyzed for hair germ markers (Lef1 and P-cadherin) and proliferation status.
At the end of the sensitization protocol, mice were sacrificed and skin samples of the treatment area were taken using biopsy punches (kai medical; kai Europe GmbH, Solingen, Germany) from each mouse.
Skin samples from 70% of mice fed upon by WT-infected nymphs were culture positive, while all skin samples from mice fed upon by the bba64 mutant-colonized nymphs were culture negative (Table 2).
To gain insight of the gene expression profile that may be involved in protection against DNA damage induced by UVB irradiation in Cbl-b−/− mice, we isolated RNA from skin samples taken before and 24 h after UVB irradiation of Cbl-b−/− and WT mice to carry out microarray analyses.
