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 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

Biogerontology

journal_title

Biogerontology

authors

Hause F,Schlote D,Simm A,Hoffmann K,Santos AN

doi

10.1007/s10522-017-9733-5

subject

Has Abstract

pub_date

2018-02-01 00:00:00

pages

95-100

issue

1

eissn

1389-5729

issn

1573-6768

pii

10.1007/s10522-017-9733-5

journal_volume

19

pub_type

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