Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0036690 (
sepsis
)
59,461
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Sepsis
induces a net catabolic state in gastrocnemius by increasing protein degradation and decreasing protein synthesis. To determine whether or not
sepsis
induces a preferential effect on the expression of individual proteins, proteins from gastrocnemius muscle of control and septic rats were separated by two-dimensional isoelectric focusing/sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Laser densitometry of proteins stained with silver provided evidence that the relative abundance of thirty-five proteins was significantly (p < .05) and reproducibly increased during
sepsis
compared to control. No individual protein underwent significant down-regulation in their relative abundance during
sepsis
. Twenty-three of the 35 proteins identified in two-dimensional gels of the gastrocnemius were also present in the plasma of septic rats. The remaining 12 proteins, therefore, were taken to represent skeletal muscle proteins. One of the 12 proteins was identified by immunoblot analysis to be
carbonic anhydrase III
. Another of the proteins was identified as triosephosphate isomerase based upon microsequencing of the N terminus.
...
PMID:Altered expression of skeletal muscle proteins during sepsis. 774 46
1.
Sepsis
is associated with marked changes in cardiac muscle protein synthesis. Such changes may be the result of altered transcription of specific myofibrillar protein mRNAs. 2. In order to investigate myofibrillar protein gene expression, a rat model of
sepsis
was used. Adult rats were given a single sub-lethal dose of lipopolysaccharide by the intraperitoneal route. At various times thereafter, rats were killed and ventricular muscle was removed. RNA was extracted and transferred to nylon membranes. Changes in expression of mRNA for alpha- and beta-myosin heavy chain, alpha-actin, cardiac troponin C and
carbonic anhydrase III
were detected by Northern hybridization. 3. After treatment with lipopolysaccharide, mRNA for beta-myosin heavy chain increased to 260% of control values at 24 h and reached a maximum of 310% at 48 h. alpha-Myosin heavy chain mRNA levels fell to 72% of control values at 24 h. mRNA levels for alpha-actin, cardiac troponin C and
carbonic anhydrase III
remained unchanged. 4. In order to investigate the role of tumour necrosis factor-alpha in this process, some rats were pretreated with monoclonal antibody against tumour necrosis factor-alpha before receiving lipopolysaccharide. Such animals showed an absence of tumour necrosis factor-alpha bioactivity in plasma, but changes in myocardial protein mRNA levels were no different from those seen in animals receiving lipopolysaccharide alone. 5. The reduction in protein synthesis in cardiac muscle in
sepsis
does not appear to be the result of reduced expression of genes for structural or soluble muscle protein.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Cardiac muscle protein gene expression in the endotoxin-treated rat. 787 42
Sepsis
is associated with net breakdown of skeletal muscle protein, mediated partly by reduced rates of muscle protein synthesis. This study investigated the role of altered gene expression for specific muscle proteins in mediating reduced protein synthesis in a rat model of acute severe
sepsis
. Adult rats were given a single sublethal intraperitoneal dose of endotoxin (bacterial lipopolysaccharide). Protein, RNA and DNA contents of muscle were measured and changes in expression of mRNA in tibialis anterior and extensor digitorum longus muscles were detected by quantification of Northern blots at 6, 24, 48 and 72 hr after endotoxin and in animals starved for 24 hr. Results showed that at 24 hr after endotoxin there was a loss of about 14% of muscle protein content. No reduction in mRNA was found at any time point for beta-myosin heavy chain (MHC), fast-MHC, alpha-actin, skeletal muscle troponin or
carbonic anhydrase III
(CA III); rather, at 48 hr there was increased expression of beta-MHC (224 +/- 123% control) and CA III (202 +/- 56%). Blocking TNF-alpha by pre-treatment with a monoclonal antibody did not appear to influence this. Total RNA content of muscle was reduced to 67% of the control values 24 hr after LPS, although this was no different to pair-fed animals starved for 24 hr. It is concluded that reduced protein synthesis in skeletal muscle in early acute
sepsis
is not primarily associated with reduced muscle protein gene expression.
...
PMID:The effect of endotoxin on skeletal muscle protein gene expression in the rat. 869 96