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Procalcitonin Impairs Liver Cell Viability and Function In Vitro: A Potential New Mechanism of Liver Dysfunction and Failure during Sepsis?

Abstract Purpose. Liver dysfunction and failure are severe complications of sepsis and result in poor outcome and increased mortality. The underlying pathologic mechanisms of hepatocyte dysfunction and necrosis during sepsis are only incompletely understood. Here, we investigated whether procalcitonin, a biomarker of sepsis, modulates liver cell function and viability. Materials and Methods. Employing a previously characterized and patented biosensor system evaluating hepatocyte toxicity in vitro, human hepatocellular carcinoma cells (HepG2/C3A) were exposed to 0.01-50 ng/mL procalcitonin for 2 × 72 h and evaluated for proliferation, necrosis, metabolic activity, cellular integrity, microalbumin synthesis, and detoxification capacity. Acetaminophen served as positive control. For further standardization, procalcitonin effects were confirmed in a cellular toxicology assay panel employing L929 fibroblasts. Data were analyzed using ANOVA/Tukey's test. Results. Already at concentrations as low as 0.25 ng/mL, procalcitonin induced HepG2/C3A necrosis (P < 0.05) and reduced metabolic activity, cellular integrity, synthesis, and detoxification capacity (all P < 0.001). Comparable effects were obtained employing L929 fibroblasts. Conclusion. We provide evidence for procalcitonin to directly impair function and viability of human hepatocytes and exert general cytotoxicity in vitro. Therapeutical targeting of procalcitonin could thus display a novel approach to reduce incidence of liver dysfunction and failure during sepsis and lower morbidity and mortality of septic patients.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28255555
OWN - NLM
STAT- MEDLINE
DA  - 20170303
DCOM- 20170313
LR  - 20170313
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Procalcitonin Impairs Liver Cell Viability and Function In Vitro: A Potential New
      Mechanism of Liver Dysfunction and Failure during Sepsis?
PG  - 6130725
LID - 10.1155/2017/6130725 [doi]
AB  - Purpose. Liver dysfunction and failure are severe complications of sepsis and
      result in poor outcome and increased mortality. The underlying pathologic
      mechanisms of hepatocyte dysfunction and necrosis during sepsis are only
      incompletely understood. Here, we investigated whether procalcitonin, a biomarker
      of sepsis, modulates liver cell function and viability. Materials and Methods.
      Employing a previously characterized and patented biosensor system evaluating
      hepatocyte toxicity in vitro, human hepatocellular carcinoma cells (HepG2/C3A)
      were exposed to 0.01-50 ng/mL procalcitonin for 2 x 72 h and evaluated for
      proliferation, necrosis, metabolic activity, cellular integrity, microalbumin
      synthesis, and detoxification capacity. Acetaminophen served as positive control.
      For further standardization, procalcitonin effects were confirmed in a cellular
      toxicology assay panel employing L929 fibroblasts. Data were analyzed using
      ANOVA/Tukey's test. Results. Already at concentrations as low as 0.25 ng/mL,
      procalcitonin induced HepG2/C3A necrosis (P &lt; 0.05) and reduced metabolic
      activity, cellular integrity, synthesis, and detoxification capacity (all P &lt;
      0.001). Comparable effects were obtained employing L929 fibroblasts. Conclusion. 
      We provide evidence for procalcitonin to directly impair function and viability
      of human hepatocytes and exert general cytotoxicity in vitro. Therapeutical
      targeting of procalcitonin could thus display a novel approach to reduce
      incidence of liver dysfunction and failure during sepsis and lower morbidity and 
      mortality of septic patients.
FAU - Sauer, Martin
AU  - Sauer M
AUID- ORCID: 0000-0001-6221-9081
AD  - Clinic for Anesthesiology and Intensive Care Medicine, University Hospital
      Rostock, Rostock, Germany; Fraunhofer Institute for Cell Therapy and Immunology, 
      EXIM, Rostock, Germany.
FAU - Doss, Sandra
AU  - Doss S
AUID- ORCID: 0000-0001-9727-1605
AD  - Fraunhofer Institute for Cell Therapy and Immunology, EXIM, Rostock, Germany.
FAU - Ehler, Johannes
AU  - Ehler J
AD  - Clinic for Anesthesiology and Intensive Care Medicine, University Hospital
      Rostock, Rostock, Germany.
FAU - Mencke, Thomas
AU  - Mencke T
AUID- ORCID: 0000-0002-9179-4437
AD  - Clinic for Anesthesiology and Intensive Care Medicine, University Hospital
      Rostock, Rostock, Germany.
FAU - Wagner, Nana-Maria
AU  - Wagner NM
AD  - Clinic for Anesthesiology and Intensive Care Medicine, University Hospital
      Rostock, Rostock, Germany.
LA  - eng
PT  - Journal Article
DEP - 20170201
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 9007-12-9 (Calcitonin)
SB  - IM
MH  - Calcitonin/*metabolism
MH  - Cell Count
MH  - Cell Death
MH  - Cell Line
MH  - Cell Survival
MH  - Hepatocytes/metabolism/pathology
MH  - Humans
MH  - Inactivation, Metabolic
MH  - Liver/metabolism/*pathology/*physiopathology
MH  - Liver Diseases/*etiology/*metabolism
MH  - Sepsis/*complications/*metabolism
PMC - PMC5309405
COI - All authors declare no actual or potential conflicts of interests.
EDAT- 2017/03/04 06:00
MHDA- 2017/03/14 06:00
CRDT- 2017/03/04 06:00
PHST- 2016/11/12 [received]
PHST- 2017/01/05 [revised]
PHST- 2017/01/10 [accepted]
AID - 10.1155/2017/6130725 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:6130725. doi: 10.1155/2017/6130725. Epub 2017 Feb 1.

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