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Experimental polymicrobial peritonitis-associated transcriptional regulation of murine endogenous retroviruses.

Abstract Despite advancements in understanding the pathophysiology of sepsis, clinical outcomes are variable, and the mortality rate remains high among patients. We investigated whether expression of murine endogenous retroviruses (MuERVs), constituting approximately 10% of the mouse genome, is differentially regulated in response to sepsis-elicited stress signals. ICR mice were subjected to cecal ligation and puncture, and MuERV expression was examined. There was evident regulation (induced or repressed) of MuERV expression in the liver and lung after cecal ligation and puncture. In particular, expression of several variant transcripts was increased, primarily in the liver, at 12 and/or 48 h: nine splicing variants and one 5.06-kb nonspliced transcript. Four novel splicing signals were also identified. Six variant transcripts were presumed to be splicing products of the 5.06-kb transcript, whereas the other three were envelope variants transcribed from at least five MuERV loci. These findings demonstrate that expression of certain MuERVs, including their envelope subgenomic transcripts, are altered during the course of sepsis pathogenesis.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title shock (augusta, ga.)
Publication Year Start
%A Cho, Kiho; Chiu, Sophia; Lee, Young-Kwan; Greenhalgh, David; Nemzek, Jean
%T Experimental polymicrobial peritonitis-associated transcriptional regulation of murine endogenous retroviruses.
%J Shock (Augusta, Ga.), vol. 32, no. 2, pp. 147-158
%D 08/2009
%V 32
%N 2
%M eng
%B Despite advancements in understanding the pathophysiology of sepsis, clinical outcomes are variable, and the mortality rate remains high among patients. We investigated whether expression of murine endogenous retroviruses (MuERVs), constituting approximately 10% of the mouse genome, is differentially regulated in response to sepsis-elicited stress signals. ICR mice were subjected to cecal ligation and puncture, and MuERV expression was examined. There was evident regulation (induced or repressed) of MuERV expression in the liver and lung after cecal ligation and puncture. In particular, expression of several variant transcripts was increased, primarily in the liver, at 12 and/or 48 h: nine splicing variants and one 5.06-kb nonspliced transcript. Four novel splicing signals were also identified. Six variant transcripts were presumed to be splicing products of the 5.06-kb transcript, whereas the other three were envelope variants transcribed from at least five MuERV loci. These findings demonstrate that expression of certain MuERVs, including their envelope subgenomic transcripts, are altered during the course of sepsis pathogenesis.
%K Animals, Endogenous Retroviruses, Female, Gene Expression Regulation, Viral, Genome, Liver, Lung, Mice, Mice, Inbred ICR, Peritonitis, RNA Splicing, RNA, Viral, Stress, Physiological, Transcription, Genetic
%P 147
%L 158
%Y 10.1097/SHK.0b013e31819721ae
%W PHY
%G AUTHOR
%R 2009.......32..147C

@Article{Cho2009,
author="Cho, Kiho
and Chiu, Sophia
and Lee, Young-Kwan
and Greenhalgh, David
and Nemzek, Jean",
title="Experimental polymicrobial peritonitis-associated transcriptional regulation of murine endogenous retroviruses.",
journal="Shock (Augusta, Ga.)",
year="2009",
month="Aug",
volume="32",
number="2",
pages="147--158",
keywords="Animals",
keywords="Endogenous Retroviruses",
keywords="Female",
keywords="Gene Expression Regulation, Viral",
keywords="Genome",
keywords="Liver",
keywords="Lung",
keywords="Mice",
keywords="Mice, Inbred ICR",
keywords="Peritonitis",
keywords="RNA Splicing",
keywords="RNA, Viral",
keywords="Stress, Physiological",
keywords="Transcription, Genetic",
abstract="Despite advancements in understanding the pathophysiology of sepsis, clinical outcomes are variable, and the mortality rate remains high among patients. We investigated whether expression of murine endogenous retroviruses (MuERVs), constituting approximately 10\% of the mouse genome, is differentially regulated in response to sepsis-elicited stress signals. ICR mice were subjected to cecal ligation and puncture, and MuERV expression was examined. There was evident regulation (induced or repressed) of MuERV expression in the liver and lung after cecal ligation and puncture. In particular, expression of several variant transcripts was increased, primarily in the liver, at 12 and/or 48 h: nine splicing variants and one 5.06-kb nonspliced transcript. Four novel splicing signals were also identified. Six variant transcripts were presumed to be splicing products of the 5.06-kb transcript, whereas the other three were envelope variants transcribed from at least five MuERV loci. These findings demonstrate that expression of certain MuERVs, including their envelope subgenomic transcripts, are altered during the course of sepsis pathogenesis.",
issn="1540-0514",
doi="10.1097/SHK.0b013e31819721ae",
url="http://www.ncbi.nlm.nih.gov/pubmed/19060780",
language="eng"
}

%0 Journal Article
%T Experimental polymicrobial peritonitis-associated transcriptional regulation of murine endogenous retroviruses.
%A Cho, Kiho
%A Chiu, Sophia
%A Lee, Young-Kwan
%A Greenhalgh, David
%A Nemzek, Jean
%J Shock (Augusta, Ga.)
%D 2009
%8 Aug
%V 32
%N 2
%@ 1540-0514
%G eng
%F Cho2009
%X Despite advancements in understanding the pathophysiology of sepsis, clinical outcomes are variable, and the mortality rate remains high among patients. We investigated whether expression of murine endogenous retroviruses (MuERVs), constituting approximately 10% of the mouse genome, is differentially regulated in response to sepsis-elicited stress signals. ICR mice were subjected to cecal ligation and puncture, and MuERV expression was examined. There was evident regulation (induced or repressed) of MuERV expression in the liver and lung after cecal ligation and puncture. In particular, expression of several variant transcripts was increased, primarily in the liver, at 12 and/or 48 h: nine splicing variants and one 5.06-kb nonspliced transcript. Four novel splicing signals were also identified. Six variant transcripts were presumed to be splicing products of the 5.06-kb transcript, whereas the other three were envelope variants transcribed from at least five MuERV loci. These findings demonstrate that expression of certain MuERVs, including their envelope subgenomic transcripts, are altered during the course of sepsis pathogenesis.
%K Animals
%K Endogenous Retroviruses
%K Female
%K Gene Expression Regulation, Viral
%K Genome
%K Liver
%K Lung
%K Mice
%K Mice, Inbred ICR
%K Peritonitis
%K RNA Splicing
%K RNA, Viral
%K Stress, Physiological
%K Transcription, Genetic
%U http://dx.doi.org/10.1097/SHK.0b013e31819721ae
%U http://www.ncbi.nlm.nih.gov/pubmed/19060780
%P 147-158

PT Journal
AU Cho, K
   Chiu, S
   Lee, Y
   Greenhalgh, D
   Nemzek, J
TI Experimental polymicrobial peritonitis-associated transcriptional regulation of murine endogenous retroviruses.
SO Shock (Augusta, Ga.)
JI Shock
PD Aug
PY 2009
BP 147
EP 158
VL 32
IS 2
DI 10.1097/SHK.0b013e31819721ae
LA eng
DE Animals; Endogenous Retroviruses; Female; Gene Expression Regulation, Viral; Genome; Liver; Lung; Mice; Mice, Inbred ICR; Peritonitis; RNA Splicing; RNA, Viral; Stress, Physiological; Transcription, Genetic
AB Despite advancements in understanding the pathophysiology of sepsis, clinical outcomes are variable, and the mortality rate remains high among patients. We investigated whether expression of murine endogenous retroviruses (MuERVs), constituting approximately 10% of the mouse genome, is differentially regulated in response to sepsis-elicited stress signals. ICR mice were subjected to cecal ligation and puncture, and MuERV expression was examined. There was evident regulation (induced or repressed) of MuERV expression in the liver and lung after cecal ligation and puncture. In particular, expression of several variant transcripts was increased, primarily in the liver, at 12 and/or 48 h: nine splicing variants and one 5.06-kb nonspliced transcript. Four novel splicing signals were also identified. Six variant transcripts were presumed to be splicing products of the 5.06-kb transcript, whereas the other three were envelope variants transcribed from at least five MuERV loci. These findings demonstrate that expression of certain MuERVs, including their envelope subgenomic transcripts, are altered during the course of sepsis pathogenesis.
ER

PMID- 19060780
OWN - NLM
STAT- MEDLINE
DA  - 20090716
DCOM- 20091001
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 32
IP  - 2
DP  - 2009 Aug
TI  - Experimental polymicrobial peritonitis-associated transcriptional regulation of
      murine endogenous retroviruses.
PG  - 147-58
LID - 10.1097/SHK.0b013e31819721ae [doi]
AB  - Despite advancements in understanding the pathophysiology of sepsis, clinical
      outcomes are variable, and the mortality rate remains high among patients. We
      investigated whether expression of murine endogenous retroviruses (MuERVs),
      constituting approximately 10% of the mouse genome, is differentially regulated
      in response to sepsis-elicited stress signals. ICR mice were subjected to cecal
      ligation and puncture, and MuERV expression was examined. There was evident
      regulation (induced or repressed) of MuERV expression in the liver and lung after
      cecal ligation and puncture. In particular, expression of several variant
      transcripts was increased, primarily in the liver, at 12 and/or 48 h: nine
      splicing variants and one 5.06-kb nonspliced transcript. Four novel splicing
      signals were also identified. Six variant transcripts were presumed to be
      splicing products of the 5.06-kb transcript, whereas the other three were
      envelope variants transcribed from at least five MuERV loci. These findings
      demonstrate that expression of certain MuERVs, including their envelope
      subgenomic transcripts, are altered during the course of sepsis pathogenesis.
FAU - Cho, Kiho
AU  - Cho K
AD  - Burn Research, Shriners Hospitals for Children Northern California, Sacramento,
      CA 95817, USA. [email protected]
FAU - Chiu, Sophia
AU  - Chiu S
FAU - Lee, Young-Kwan
AU  - Lee YK
FAU - Greenhalgh, David
AU  - Greenhalgh D
FAU - Nemzek, Jean
AU  - Nemzek J
LA  - eng
GR  - GM067189/GM/NIGMS NIH HHS/United States
GR  - GM5486/GM/NIGMS NIH HHS/United States
GR  - R01GM071360/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (RNA, Viral)
SB  - IM
MH  - Animals
MH  - Endogenous Retroviruses/*immunology/metabolism
MH  - Female
MH  - Gene Expression Regulation, Viral/*immunology
MH  - Genome/immunology
MH  - Liver/*immunology/virology
MH  - Lung/*immunology/virology
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Peritonitis/*immunology/virology
MH  - RNA Splicing/immunology
MH  - RNA, Viral/immunology
MH  - Stress, Physiological/immunology
MH  - Transcription, Genetic/*immunology
EDAT- 2008/12/09 09:00
MHDA- 2009/10/02 06:00
CRDT- 2008/12/09 09:00
AID - 10.1097/SHK.0b013e31819721ae [doi]
PST - ppublish
SO  - Shock. 2009 Aug;32(2):147-58. doi: 10.1097/SHK.0b013e31819721ae.

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