PMID- 25559736
OWN - NLM
STAT- MEDLINE
DCOM- 20160126
LR  - 20181113
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 1
DP  - 2015
TI  - The restrained expression of NF-kB in renal tissue ameliorates folic acid induced 
      acute kidney injury in mice.
PG  - e115947
LID - 10.1371/journal.pone.0115947 [doi]
LID - e115947
AB  - The Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) 
      represent family of structurally-related eukaryotic transcription factors which 
      regulate diverse array of cellular processes including immunological responses, 
      inflammation, apoptosis, growth & development. Increased expression of NF-kB has 
      often been seen in many diverse diseases, suggesting the importance of genomic 
      deregulation to disease pathophysiology. In the present study we focused on acute 
      kidney injury (AKI), which remains one of the major risk factor showing a high 
      rate of mortality and morbidity. The pathology associated with it, however, 
      remains incompletely known though inflammation has been reported to be one of the 
      major risk factor in the disease pathophysiology. The role of NF-kB thus seemed 
      pertinent. In the present study we show that high dose of folic acid (FA) induced 
      acute kidney injury (AKI) characterized by elevation in levels of blood urea 
      nitrogen & serum creatinine together with extensive tubular necrosis, loss of 
      brush border and marked reduction in mitochondria. One of the salient 
      observations of this study was a coupled increase in the expression of renal, 
      relA, NF-kB2, and p53 genes and proteins during folic acid induced AKI (FA AKI). 
      Treatment of mice with NF-kB inhibitor, pyrrolidine dithio-carbamate ammonium 
      (PDTC) lowered the expression of these transcription factors and ameliorated the 
      aberrant renal function by decreasing serum creatinine levels. In conclusion, our 
      results suggested that NF-kB plays a pivotal role in maintaining renal function 
      that also involved regulating p53 levels during FA AKI.
FAU - Kumar, Dev
AU  - Kumar D
AD  - Department of Biochemistry, Panjab University, Chandigarh, India.
FAU - Singla, Surinder K
AU  - Singla SK
AD  - Department of Biochemistry, Panjab University, Chandigarh, India.
FAU - Puri, Veena
AU  - Puri V
AD  - Centre for Systems Biology & Bioinformatics, Panjab University, Chandigarh, 
      India.
FAU - Puri, Sanjeev
AU  - Puri S
AD  - Biotechnology Branch, University Institute of Engineering & Technology, Panjab 
      University, Chandigarh, India; Centre for Stem Cell & Tissue Engineering, Panjab 
      University, Chandigarh, India.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150105
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antioxidants)
RN  - 0 (NF-kappa B)
RN  - 0 (NF-kappa B p52 Subunit)
RN  - 0 (Pyrrolidines)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Thiocarbamates)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - 935E97BOY8 (Folic Acid)
SB  - IM
MH  - Acute Kidney Injury/chemically induced/*genetics/metabolism
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Folic Acid
MH  - *Gene Expression
MH  - Immunohistochemistry
MH  - Kidney/drug effects/*metabolism/pathology
MH  - Kidney Cortex/metabolism/pathology/ultrastructure
MH  - Kidney Function Tests
MH  - Male
MH  - Mice, Inbred BALB C
MH  - Microscopy, Electron, Transmission
MH  - NF-kappa B/antagonists & inhibitors/*genetics/metabolism
MH  - NF-kappa B p52 Subunit/antagonists & inhibitors/genetics/metabolism
MH  - Pyrrolidines/pharmacology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Thiocarbamates/pharmacology
MH  - Transcription Factor RelA/antagonists & inhibitors/genetics/metabolism
MH  - Tumor Suppressor Protein p53/genetics/metabolism
PMC - PMC4283964
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/01/07 06:00
MHDA- 2016/01/27 06:00
PMCR- 2015/01/05
CRDT- 2015/01/07 06:00
PHST- 2014/09/07 00:00 [received]
PHST- 2014/11/27 00:00 [accepted]
PHST- 2015/01/07 06:00 [entrez]
PHST- 2015/01/07 06:00 [pubmed]
PHST- 2016/01/27 06:00 [medline]
PHST- 2015/01/05 00:00 [pmc-release]
AID - PONE-D-14-39208 [pii]
AID - 10.1371/journal.pone.0115947 [doi]
PST - epublish
SO  - PLoS One. 2015 Jan 5;10(1):e115947. doi: 10.1371/journal.pone.0115947. 
      eCollection 2015.