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 ic J /ic J mice displaying skin defects similar to those of classical progeria. Therefore, we analysed AGE-modifications in protein extracts from various tissues of ic J /ic J mice. Our results demonstrated that pentosidine as well as argpyrimidine were increased in ic J /ic J 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 ic J /ic J and control mice. The results indicate that not only lamin A but also the lamin B receptor may be involved in ageing processes.
journal_name
Biogerontologyjournal_title
Biogerontologyauthors
Hause F,Schlote D,Simm A,Hoffmann K,Santos ANdoi
10.1007/s10522-017-9733-5subject
Has Abstractpub_date
2018-02-01 00:00:00pages
95-100issue
1eissn
1389-5729issn
1573-6768pii
10.1007/s10522-017-9733-5journal_volume
19pub_type
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