Fig 1: Mvd ablation in keratinocytes‐induced skin lesions. (A) Mvd was ablated in keratinocytes by intraperitoneal TAM injection. All samples were harvested at Day 90. (B) The body weight of WT and Mvd KO/KO mice. The weight of both groups of mice decreased during the injection period and gradually increased thereafter. (C) Mvd KO/KO mice showed skin lesions of ears, paws, and tails in the second week. These lesions continued to deteriorate until the fourth week. The WT group showed no abnormality. Mvd indicates mevalonate diphosphate decarboxylase; WT, wild type.
Fig 2: Mvd deficiency in the epidermis activated lipid metabolism. (A) Heat map analysis of genes related to lipid metabolism. (B) WB analysis of the epidermis revealed the upregulated level of FABP5 and PLA2G4E protein expression. The data are performed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 by using student's t‐test. Mvd indicates mevalonate diphosphate decarboxylase; WT, wild type.
Fig 3: Mvd deficiency in the epidermis led to PK pathological manifestations. Histopathology of ear, paw, and tail skin. Mvd KO/KO mice showed characteristic PK manifestation of cornoid lamella, which is a tightly packed thin column of parakeratotic cells overlying a zone of focal hypogranulosis. The presence of dyskeratotic keratinocytes and lymphocytic inflammation in the dermis could also be observed. Mvd indicates mevalonate diphosphate decarboxylase; WT, wild type.
Fig 4: Construction and generation of transgenetic K14‐CreERT2‐Mvd fl/fl mouse. (A) The targeting vector sequence was comprised of a 3.0 kb 5′ homologous arm, a 2.1 kb flox region, PGK‐Neo‐polyA, a 3.0 kb 3′ homologous arm, and a MC1‐TK‐polyA negative screening marker. (B) The strategy of gene editing. (C) Mouse homozygous for LoxP flanked gene of Mvd was crossed with mouse expressing K14‐specific Cre. After two generations, Mvd KO/KO mouse was obtained. Mvd indicates mevalonate diphosphate decarboxylase.
Fig 5: Mvd deficiency in the epidermis led to obvious inflammation and epidermal barrier damage. (A) WB analysis of the epidermis revealed the reduced level of Mvd protein expression and the upregulated level of IL‐1β and IL‐17A. (B) Immunohistochemistry for Mvd, IL‐17A, and Loricrin of ear skin (Scale bars, 100 µm). The data are performed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 by using student's t‐test. Mvd indicates mevalonate diphosphate decarboxylase; WT, wild type.
Supplier Page from Abcam for Anti-MVD antibody