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Published in: Inflammation Research 10/2013

01-10-2013 | Original Research Paper

Procalcitonin induced cytotoxicity and apoptosis in mesangial cells: implications for septic renal injury

Authors: Magali Araujo, Sonia Q. Doi, Carlos E. Palant, Eric S. Nylen, Kenneth L. Becker

Published in: Inflammation Research | Issue 10/2013

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Abstract

Objective and design

Immuno-neutralization of procalcitonin (ProCT) has been shown to ameliorate experimental sepsis as well as the renal complications of this disease. Accordingly, we investigated the direct effect of ProCT on mesangial cells (MCs).

Material

Primary culture of murine MCs.

Treatment

ProCT (0.5, 1.0, 2.5, 5.0 ng/ml) for 2, 4, 6 h.

Methods

MCs were exposed in vitro to ProCT. Expression levels of IL-6, iNOS and TNF-α were determined by real time RT-PCR, Inflammatory pathways, and a panel of cytokines and chemokines involved in the process were investigated by PCR array; apoptosis/viability were evaluated in a multiplex assay and actin cytoskeleton alterations were examined by immunofluorescence (IF).

Results

ProCT caused an early elevation in both IL-6 and iNOS mRNA (2–4 h), and a later rise (6 h) in TNF-α mRNA. ProCT upregulated genes of proinflammatory pathways 5- to 24-fold compared to control. IF images revealed disruption of the actin cytoskeleton and retraction of cell bodies with loss of typical stellate or spindle shape phenotype. ProCT decreased MCs viability by 36 % compared to control cells and induced significant apoptosis.

Conclusions

ProCT has direct cytotoxic properties and may play a role in septic acute kidney injury that is independent of endotoxemia or hemodynamic alterations.
Appendix
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Metadata
Title
Procalcitonin induced cytotoxicity and apoptosis in mesangial cells: implications for septic renal injury
Authors
Magali Araujo
Sonia Q. Doi
Carlos E. Palant
Eric S. Nylen
Kenneth L. Becker
Publication date
01-10-2013
Publisher
Springer Basel
Published in
Inflammation Research / Issue 10/2013
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-013-0646-8

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