Vimentin cleavage in end-stage renal disease is not related to apoptosis

• Authors: Felix Liebscher , Tobias Arnold , Ying Liang , Thomas Reiter , Georg Böhmig , Rudolf Oehler
• Languages of publication: EN

Abstracts

EN

Anti-vimentin auto-antibodies contribute to chronic allograft nephropathy. They exist in sera of end-stage renal disease patients on hemodialysis (ESRD) already before renal transplantation. We found recently that a 49 kDa vimentin fragment is increased in lymphocytes of ESRD patients which is presented on the cell surface. In vitro studies showed that such a fragment is formed during apoptosis by active caspase-3. We hypothesized that vimentin degradation in leukocytes of ESRD patients correlates to caspase-3 activation in vivo. Lymphocytes and monocytes were isolated from ESRD patients and from healthy volunteers and analyzed for vimentin expression and caspase-3 activation. In addition, apoptosis was induced in vitro and quantified by flow cytometry. ESRD monocytes have shown only the full length 60 kDa vimentin isoform. ESRD lymphocytes, however, showed in addition a strongly increased expression of the 49 kDa vimentin in all samples. Caspase-3 activation was found in 60% of ESRD lymphocytes and 66% of ESRD monocytes but not in healthy volunteers. UV-mediated induction of apoptosis was not associated with vimentin degradation. These experiments could confirm increased vimentin degradation in ESRD lymphocytes. However, we could not validate any correlation to apoptosis.

Keywords

EN

Vimentin; Apoptosis; Caspase-3; End-stage renal disease

• Publisher: De Gruyter Open
• Journal: Open Medicine
• Year: 2013
• Volume: 8
• Issue: 3
• Pages: 297-301

Dates

published

1 - 6 - 2013

online

17 - 4 - 2013

Contributors

author

Felix Liebscher

• Department of Surgery, Medical University of Vienna, A-1090, Vienna, Austria

author

Tobias Arnold

• Department of Surgery, Medical University of Vienna, A-1090, Vienna, Austria

author

Ying Liang

• Department of Surgery, Medical University of Vienna, A-1090, Vienna, Austria

author

Thomas Reiter

• Department of Internal Medicine-I, Medical University of Vienna, A-1090, Vienna, Austria

author

Georg Böhmig

• Department of Internal Medicine-I, Medical University of Vienna, A-1090, Vienna, Austria

author

Rudolf Oehler

• Department of Surgery, Medical University of Vienna, A-1090, Vienna, Austria

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Identifiers

DOI

10.2478/s11536-012-0131-8