Biogerontology

, Volume 19, Issue 1, pp 95–100 | Cite as

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

  • Frank Hause
  • Dietmar Schlote
  • Andreas Simm
  • Katrin Hoffmann
  • Alexander Navarrete Santos
Rapid Communication

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.

Keywords

Lbr deficiency Premature ageing Advanced glycation endproducts Gene expression 

Notes

Acknowledgements

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

Compliance with ethical standard

Conflict of interest

The authors declare no conflict of interest.

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Copyright information

© Springer Science+Business Media B.V. 2017

Authors and Affiliations

  1. 1.Institute for Human GeneticsMartin Luther University of Halle-WittenbergHalleGermany
  2. 2.Clinic for Cardiac und Thoracic SurgeryMartin Luther University of Halle-WittenbergHalleGermany

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