Accumulation of glycated proteins suggesting premature ageing in lamin B receptor deficient mice

Abstract

Accumulation of advanced glycation end products (AGEs) is accompanied by increased free radical activity which contributes to ageing and the development or worsening of degenerative diseases. Apart from other physiological factors, AGEs are also an important biomarker for premature ageing. Here we report protein modifications (glycation) in a mouse model of lamin B receptor deficient icJ/icJ mice displaying skin defects similar to those of classical progeria. Therefore, we analysed AGE-modifications in protein extracts from various tissues of icJ/icJ mice. Our results demonstrated that pentosidine as well as argpyrimidine were increased in icJ/icJ mice indicating a modification specific increase in biomarkers of ageing, especially derived from glycolysis dependent methylglyoxal. Furthermore, the expression of AGE-preventing enzymes (Glo1, Fn3k) differed between icJ/icJ and control mice. The results indicate that not only lamin A but also the lamin B receptor may be involved in ageing processes.