Document Detail

Mechanism of intracellular signal transduction during injury of renal tubular cells induced by postasphyxial serum in neonates with asphyxia.
MedLine Citation:
PMID:  19204408     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Renal injury is a severe and extremely common complication that occurs early in neonates with asphyxia. Reperfusion injury has been suggested as the cause of kidney damage during resuscitation of neonatal asphyxia. Previous studies have demonstrated that postasphyxial serum from neonates with asphyxia may result in apoptosis of renal tubular cells. However, the mechanisms that mediate renal tubular cell apoptosis induced by postasphyxial serum remain poorly understood. OBJECTIVES: In this report we investigate the intracellular signal transduction mechanisms that operate during injury of renal tubular cells induced by postasphyxial serum in neonates. METHODS: Cultured human renal proximal tubular cells HK-2 cell were exposed to 10% fetal calf serum (normal control), 20% postasphyxial serum or 20% postasphyxial serum with pyrrolidine dithiocarbamate (PDTC). The expression of both BAD and BAX in the cytoplasm was detected by immunohistochemistry. The mitochondria membrane potential (Deltapsim) was examined by confocal microscopy, and the release of the apoptogenic mitochondrial proteins cytochrome C and AIF was assessed by Western blot analysis. RESULTS: Loss of mitochondria membrane potential was detected in HK-2 cells treated with 20% postasphyxial serum as compared to cells in normal serum or PTDC-pretreated cells in 20% postasphyxial serum. A significant increase of Bad and Bax protein expression was also detected, along with the release of cytochrome C and AIF from mitochondria to cytosol in the postasphyxial serum treated cells, but not in the normal or PTDC-pretreated control cells. CONCLUSIONS: Our findings suggest that postasphyxial serum may induce renal tubular cell apoptosis through the mitochondrial pathway, and its intracellular signal transduction mechanism includes the activation of nuclear factor-kappaB.
Jin Zhao; Wen-Bin Dong; Peng-yun Li; Chun-liang Deng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-02-10
Journal Detail:
Title:  Neonatology     Volume:  96     ISSN:  1661-7819     ISO Abbreviation:  -     Publication Date:  2009  
Date Detail:
Created Date:  2009-06-26     Completed Date:  2009-09-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101286577     Medline TA:  Neonatology     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  33-42     Citation Subset:  IM    
Copyright Information:
Copyright 2009 S. Karger AG, Basel.
Department of Newborn Medicine, Affiliated Hospital of Luzhou Medical College, Luzhou 646000, PR China.
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MeSH Terms
Asphyxia Neonatorum / blood*,  complications*,  therapy
Cell Line
Cytochromes c / secretion
Cytoplasm / chemistry
Infant, Newborn
Kidney Diseases / etiology*,  pathology,  physiopathology
Kidney Tubules*
Kidney Tubules, Proximal / ultrastructure
Membrane Potential, Mitochondrial
NF-kappa B / antagonists & inhibitors
Pyrrolidines / administration & dosage
Reperfusion Injury / etiology*
Signal Transduction / physiology*
Thiocarbamates / administration & dosage
bcl-2-Associated X Protein / analysis
bcl-Associated Death Protein / analysis
Reg. No./Substance:
0/NF-kappa B; 0/Pyrrolidines; 0/Thiocarbamates; 0/bcl-2-Associated X Protein; 0/bcl-Associated Death Protein; 25769-03-3/pyrrolidine dithiocarbamic acid; 9007-43-6/Cytochromes c

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