Extended Data Fig. 3: miR-31 up-regulation in skin epithelium induces HFSC transepidermal differentiation and aging-like phenotypes.
From: A stress-induced miR-31–CLOCK–ERK pathway is a key driver and therapeutic target for skin aging
a, miR-31 qRT-PCR of young/old/WT/DTG backskin epidermis. n = 3 biologically independent mice each. WT/DTG mice were induced by Dox at P48 and samples collected 2 days later. b, Backskin photographs of WT/DTG littermates at age P48 and P62 without Dox induction. Scale bars: 1 cm. c, IF staining images of the above DTG and WT backskin sections. DAPI is in blue. Scale bars: 50 μm. d, IF staining images of backskin sections of P55 WT/DTG littermates (+Dox since P21). Arrow heads: K10 and LOR signals in HF. Scale bars: 50 μm. CD49f is in Red. DAPI is in blue. e, Left diagram: Schematic of full-thickness wound healing assay procedures in Dox induced WT/DTG mice. The mice were Dox induced at P48 and wounded at P50. Middle: Photographs of the wound healing process. Scale bars: 5 mm. Right: Quantification of the wound healing process in E Figure. Vertical axis: % wound healed. n = 6 biologically independent mice. f, Left panel: white-field images of day 4 exoplant cultures of backskin samples from DTG/WT littermates (+Dox since P48). Dashed lines: borders of MK sheet migration. #: original exoplant. Scale bars: 100 μm. Right panel: Quantification of the MK sheet area. n = 6 exoplants separated from 3 mice. g, IF staining images of full-thickness wound d7 backskin sections of P55 WT/DTG littermates (+Dox since P21). Scale bars: 200 μm. Brackets indicates open wound area. For all relevant figures, data are represented as mean ± SEM. P values were calculated with two tail t-test.
