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

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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.

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Acknowledgements

This work was part of the DFG Research Training Group 2155 (ProMoAge).

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Authors and Affiliations

  1. Institute for Human Genetics, Martin Luther University of Halle-Wittenberg, 06112, Halle, Germany

    Frank Hause, Dietmar Schlote & Katrin Hoffmann

  2. Clinic for Cardiac und Thoracic Surgery, Martin Luther University of Halle-Wittenberg, 06097, Halle, Germany

    Andreas Simm & Alexander Navarrete Santos

Authors
  1. Frank Hause
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  2. Dietmar Schlote
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  3. Andreas Simm
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  4. Katrin Hoffmann
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  5. Alexander Navarrete Santos
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Correspondence to Dietmar Schlote.

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Hause, F., Schlote, D., Simm, A. et al. Accumulation of glycated proteins suggesting premature ageing in lamin B receptor deficient mice. Biogerontology 19, 95–100 (2018). https://doi.org/10.1007/s10522-017-9733-5

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