PMID- 21698182
OWN - NLM
STAT- MEDLINE
DCOM- 20111107
LR  - 20211020
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 6
IP  - 6
DP  - 2011
TI  - Renal HIV expression is unaffected by serum LPS levels in an HIV transgenic mouse 
      model of LPS induced kidney injury.
PG  - e20688
LID - 10.1371/journal.pone.0020688 [doi]
LID - e20688
AB  - Acute kidney injury (AKI) is associated with increased rates of mortality. For 
      unknown reasons, HIV infected individuals have a higher risk of AKI than 
      uninfected persons. We tested our hypothesis that increased circulating LPS 
      increases renal expression of HIV and that HIV transgenic (Tg26) mice have 
      increased susceptibility to AKI. Tg26 mice harbor an HIV transgene encoding all 
      HIV genes except gag and pol, and develop a phenotype analogous to HIVAN. Mice 
      were used at 4-6 weeks of age before the onset of gross renal disease. Mice were 
      injected i.p. with LPS or sterile saline. Renal function, tubular injury, 
      cytokine expression, and HIV transcription were evaluated in Tg26 and wild type 
      (WT) mice. LPS injection induced a median 60.1-fold increase in HIV expression in 
      spleen but no change in kidney. There was no significant difference in renal 
      function, cytokine expression, or tubular injury scores at baseline or 24 hours 
      after LPS injection. HIV transcription was also analyzed in vitro using a human 
      renal tubular epithelial cell (RTEC) line. HIV transcription increased minimally 
      in human RTEC, by 1.47 fold, 48 hours after LPS exposure. We conclude that Tg26 
      mice do not increase HIV expression or have increased susceptibility to LPS 
      induced AKI. The increased risk of AKI in HIV infected patients is not mediated 
      via increased renal expression of HIV in the setting of sepsis. Moreover, renal 
      regulation of HIV transcription is different to that in the spleen.
FAU - Leventhal, Jeremy S
AU  - Leventhal JS
AD  - Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, 
      New York City, New York, United States of America. jeremy.leventhal@mssm.edu
FAU - Alsauskas, Zygimantas
AU  - Alsauskas Z
FAU - Snyder, Alexandra
AU  - Snyder A
FAU - Gong, Pengfei
AU  - Gong P
FAU - Wang, Bin
AU  - Wang B
FAU - D'Agati, Vivette
AU  - D'Agati V
FAU - Ross, Michael J
AU  - Ross MJ
LA  - eng
GR  - R01 DK078510/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110616
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (DNA Primers)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Cell Line
MH  - DNA Primers
MH  - *Disease Models, Animal
MH  - HIV/genetics/*isolation & purification
MH  - Kidney/*virology
MH  - Kidney Diseases/blood/*chemically induced/virology
MH  - Lipopolysaccharides/*blood
MH  - Mice
MH  - Mice, Transgenic
MH  - Transcription, Genetic
PMC - PMC3116837
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2011/06/24 06:00
MHDA- 2011/11/08 06:00
PMCR- 2011/06/16
CRDT- 2011/06/24 06:00
PHST- 2011/01/19 00:00 [received]
PHST- 2011/05/06 00:00 [accepted]
PHST- 2011/06/24 06:00 [entrez]
PHST- 2011/06/24 06:00 [pubmed]
PHST- 2011/11/08 06:00 [medline]
PHST- 2011/06/16 00:00 [pmc-release]
AID - PONE-D-11-01786 [pii]
AID - 10.1371/journal.pone.0020688 [doi]
PST - ppublish
SO  - PLoS One. 2011;6(6):e20688. doi: 10.1371/journal.pone.0020688. Epub 2011 Jun 16.