Lamin A and lamin-associated polypeptide 2 (LAP-2) in human skin fibroblasts in the process of aging

Abstract

Mutations of lamin genes lead to diseases, one of which is progeria. This disease is caused by violation of splicing of lamin A gene and accumulation of farnesylated prelamin A (progerin) in the nucleus. LAP-2 is an important factor that regulates and stabilizes the nucleoplasmic pool of lamin A. However, roles of lamin A and LAP-2 in renewal regulation of the population of fibroblasts in the human dermis in different age periods still have not been investigated. The purpose of this investigation was to define expression of lamin A and LAP-2 in human dermal fibroblasts at different ages. Lamin A and LAP-2 were detected in skin sections by indirect immunohistochemistry. It was found that the number of fibroblasts containing lamin A gradually decreased from 90.4 to 76.9% from 20 weeks of pregnancy to 85 years. It was revealed that 32% of dermal fibroblasts were positively stained for LAP-2 in the period from 20 weeks of pregnancy to 20 years, 37.8% in the period of 21–40 years, and 49–51% in the period of 41–85 years. Lamin A expression levels in fibroblast nuclei were essentially constant from 20 weeks of pregnancy to 85 years, while LAP-2 content in fibroblast nuclei was reducing from 0 to 20 years as compared with the embryonic period and was gradually increasing after 21 year. The total number of fibroblasts and PCNA-positive fibroblasts in the dermis decreased with age. The most significant decrease in the number of fibroblasts was observed from 20 weeks of pregnancy to 20 years. The results suggest involvement of lamin A and LAP-2 in the age-related decrease in the number of fibroblasts in the human dermis.

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