Relation of Skin Polyamines to the Hairless Phenotype in Transgenic Mice Overexpressing Spermidine/Spermine N1-Acetyltransferase
May 2001
in “
Journal of Investigative Dermatology
”
spermidine/spermine N1-acetyltransferase SSAT putrescine hair follicle anagen phase dermal cysts epidermal utriculi ornithine decarboxylase ODC epithelial cell proliferation follicular cysts epidermal thickening papilloma skin carcinogenesis tumor-promoting agents hair cycle hair loss skin issues hairless phenotype
TLDR Excessive putrescine causes hair loss in transgenic mice by disrupting hair follicle development.
The study examined transgenic mice overexpressing spermidine/spermine N1-acetyltransferase, which caused increased polyamine catabolism and resulted in permanent hair loss by 3 weeks of age. Although these mice completed the first hair cycle normally, they showed early hair follicle degeneration by day 15, leading to the formation of dermal cysts and epidermal utriculi. High levels of putrescine were linked to disrupted hair follicle development and the hairless phenotype. Despite this, the transgenic mice were more resistant to skin papillomas in a carcinogenesis model, suggesting that putrescine played a crucial role in hair follicle development and its overaccumulation contributed to hairlessness. Additionally, elevated putrescine and N1-acetylspermidine levels were associated with continuous epithelial cell proliferation, and the mice's resistance to tumorigenesis was possibly due to the inability of tumor-promoting agents to induce ornithine decarboxylase and expand skin spermidine pools.
