Generation of a New Rodent Model of Scleroderma

Researchers developed a new mouse model for scleroderma, characterized by skin thickening, dermal fibrosis, loss of dermal white adipose tissue, and alopecia. This model involved a 'silent' transgene randomly integrated into the mouse genome. Mice homozygous for the transgene were hairless, showing marked dermal fibrosis and absence of hair follicles, while hemizygous mice developed normally. The transgene was inserted into the keratin locus on chromosome 11, affecting a keratin not previously linked to hair growth. This model could help identify mechanisms behind dermal fibrosis and adipose tissue loss, with further studies like RNAseq planned to explore the keratin locus disruption effects.