PMID- 16109906
OWN - NLM
STAT- MEDLINE
DCOM- 20060112
LR  - 20220408
IS  - 1524-4628 (Electronic)
IS  - 0039-2499 (Linking)
VI  - 36
IP  - 9
DP  - 2005 Sep
TI  - Elevated tumor necrosis factor-alpha in skeletal muscle after stroke.
PG  - 2021-3
AB  - BACKGROUND AND PURPOSE: Tumor necrosis factor-alpha (TNF-alpha), an inflammatory 
      cytokine negligibly expressed in normal muscle, is elevated in selected metabolic 
      conditions characterized by muscle wasting and insulin resistance. Inflammation 
      is fundamental to stroke pathogenesis. Stroke patients have gross muscular 
      atrophy and high prevalence of diabetes and insulin resistance. Yet, no previous 
      studies examined TNF-alpha expression in hemiparetic skeletal muscle. This study 
      investigates whether TNF-alpha mRNA levels are elevated in paretic compared with 
      nonparetic leg muscles of chronic ischemic stroke patients and age-matched 
      controls. METHOD: Total RNA extracted from bilateral vastus lateralis muscle 
      biopsies from n=20 hemiparetic stroke patients and n=9 healthy controls was 
      reverse transcribed to cDNA, then TNF-alpha transcripts were amplified by 
      real-time quantitative polymerase chain reaction. TNF-alpha mRNA concentrations 
      were normalized against acidic ribosomal phosphoprotein, housekeeping gene. 
      RESULTS: TNF-alpha mRNA levels were 2.8-fold higher in paretic compared with 
      control leg muscle (6.28+/-1.86 versus 2.28+/-0.67; P<0.03) and 1.6-fold higher 
      in nonparetic leg (3.71+/-1.02; P<0.11) compared with controls. There was a trend 
      for higher TNF-alpha mRNA in paretic compared with nonparetic leg. CONCLUSIONS: 
      Findings demonstrate increased TNF-alpha expression in paretic leg muscle, 
      suggesting inflammatory pathways are accelerated in stroke muscle. Further 
      studies are under way to determine whether intramuscular TNF-alpha contributes to 
      atrophy and metabolic abnormalities after stroke.
FAU - Hafer-Macko, Charlene E
AU  - Hafer-Macko CE
AD  - Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 
      21201, USA. cmacko@grecc.umaryland.edu
FAU - Yu, Shuzhen
AU  - Yu S
FAU - Ryan, Alice S
AU  - Ryan AS
FAU - Ivey, Frederick M
AU  - Ivey FM
FAU - Macko, Richard F
AU  - Macko RF
LA  - eng
GR  - 1KO1AG19242-02/AG/NIA NIH HHS/United States
GR  - 1KO1NS19242-02/NS/NINDS NIH HHS/United States
GR  - P60-AG12583/AG/NIA NIH HHS/United States
GR  - R01 DK59758-01/DK/NIDDK NIH HHS/United States
GR  - R01AG19310/AG/NIA NIH HHS/United States
GR  - R29 AG14487-01/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20050818
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (DNA, Complementary)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 63231-63-0 (RNA)
SB  - IM
MH  - Aged
MH  - Atrophy/pathology
MH  - Case-Control Studies
MH  - DNA, Complementary/metabolism
MH  - Female
MH  - Gene Expression Regulation
MH  - Humans
MH  - Inflammation
MH  - Leg/pathology
MH  - Male
MH  - Middle Aged
MH  - Muscle, Skeletal/*metabolism
MH  - RNA/chemistry
MH  - RNA, Messenger/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Ribosomes/chemistry
MH  - Stroke/*metabolism/*pathology
MH  - Transcription, Genetic
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/metabolism
EDAT- 2005/08/20 09:00
MHDA- 2006/01/13 09:00
CRDT- 2005/08/20 09:00
PHST- 2005/08/20 09:00 [pubmed]
PHST- 2006/01/13 09:00 [medline]
PHST- 2005/08/20 09:00 [entrez]
AID - 01.STR.0000177878.33559.fe [pii]
AID - 10.1161/01.STR.0000177878.33559.fe [doi]
PST - ppublish
SO  - Stroke. 2005 Sep;36(9):2021-3. doi: 10.1161/01.STR.0000177878.33559.fe. Epub 2005 
      Aug 18.