, Volume 33, Issue 4, pp 543–554

Tight binding of proteins to membranes from older human cells


    • Save Sight InstituteSydney University
  • Susana Comte-Walters
    • Department of PharmacologyMedical University of South Carolina
  • Zsolt Ablonczy
    • Department of PharmacologyMedical University of South Carolina
  • John H. Schwacke
    • Department of BiochemistryMedical University of South Carolina
  • Yoke Berry
    • School of ChemistryUniversity of Wollongong
  • Anastasia Korlimbinis
    • Save Sight InstituteSydney University
  • Michael G. Friedrich
    • Save Sight InstituteSydney University
  • Kevin L. Schey
    • Mass Spectrometry Research CenterVanderbilt University

DOI: 10.1007/s11357-010-9198-9

Cite this article as:
Truscott, R.J.W., Comte-Walters, S., Ablonczy, Z. et al. AGE (2011) 33: 543. doi:10.1007/s11357-010-9198-9


The lens is an ideal model system for the study of macromolecular aging and its consequences for cellular function, since there is no turnover of lens fibre cells. To examine biochemical processes that take place in the lens and that may also occur in other long-lived cells, membranes were isolated from defined regions of human lenses that are synthesised at different times during life, and assayed for the presence of tightly bound cytosolic proteins using quantitative iTRAQ proteomics technology. A majority of lens beta crystallins and all gamma crystallins became increasingly membrane bound with age, however, the chaperone proteins alpha A and alpha B crystallin, as well as the thermally-stable protein, βB2 crystallin, did not. Other proteins such as brain-associated signal protein 1 and paralemmin 1 became less tightly bound in the older regions of the lens. It is evident that protein–membrane interactions change significantly with age. Selected proteins that were formerly cytosolic become increasingly tightly bound to cell membranes with age and are not removed even by treatment with 7 M urea. It is likely that such processes reflect polypeptide denaturation over time and the untoward binding of proteins to membranes may alter membrane properties and contribute to impairment of communication between older cells.


Human lensAgingProtein denaturationMembrane bindingLens barrier

Supplementary material

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High-resolution image (TIFF 441 kb)

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© American Aging Association 2010