Linked Life Data

20228261

Source:http://linkedlifedata.com/resource/pubmed/id/20228261

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-5-5
pubmed:abstractText
Congestive heart failure is associated with activation of the renin-angiotensin system and skeletal muscle wasting. Angiotensin II (ANG II) has been shown to increase muscle proteolysis and decrease circulating and skeletal muscle IGF-1. We have shown previously that skeletal muscle-specific overexpression of IGF-1 prevents proteolysis and apoptosis induced by ANG II. These findings indicated that downregulation of IGF-1 signaling in skeletal muscle played an important role in the wasting effect of ANG II. However, the signaling pathways and mechanisms whereby IGF-1 prevents ANG II-induced skeletal muscle atrophy are unknown. Here we show ANG II-induced transcriptional regulation of two ubiquitin ligases atrogin-1 and muscle ring finger-1 (MuRF-1) that precedes the reduction of skeletal muscle IGF-1 expression, suggesting that activation of atrogin-1 and MuRF-1 is an initial mechanism leading to skeletal muscle atrophy in response to ANG II. IGF-1 overexpression in skeletal muscle prevented ANG II-induced skeletal muscle wasting and the expression of atrogin-1, but not MuRF-1. Dominant-negative Akt and constitutively active Foxo-1 blocked the ability of IGF-1 to prevent ANG II-mediated upregulation of atrogin-1 and skeletal muscle wasting. Our findings demonstrate that the ability of IGF-1 to prevent ANG II-induced skeletal muscle wasting is mediated via an Akt- and Foxo-1-dependent signaling pathway that results in inhibition of atrogin-1 but not MuRF-1 expression. These data suggest strongly that atrogin-1 plays a critical role in mechanisms of ANG II-induced wasting in vivo.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-10200250, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-10373556, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-11175789, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-11715022, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-12690258, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-14551207, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-15109499, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-15125842, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-15479644, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-15650772, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-15661854, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-15927519, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-16228971, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-16250905, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-16265380, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-18191039, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-18467435, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-18955974, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-19158350, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-6854961, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-8647943, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-9107242, http://linkedlifedata.com/resource/pubmed/commentcorrection/20228261-9743122
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1522-1539
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
298
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1565-70
pubmed:dateRevised
2011-7-28
pubmed:meshHeading
pubmed-meshheading:20228261-Angiotensin II, pubmed-meshheading:20228261-Animals, pubmed-meshheading:20228261-Atrophy, pubmed-meshheading:20228261-Electroporation, pubmed-meshheading:20228261-Forkhead Transcription Factors, pubmed-meshheading:20228261-Gene Expression Regulation, pubmed-meshheading:20228261-Humans, pubmed-meshheading:20228261-Immunoblotting, pubmed-meshheading:20228261-Insulin-Like Growth Factor I, pubmed-meshheading:20228261-Luciferases, pubmed-meshheading:20228261-Mice, pubmed-meshheading:20228261-Mice, Inbred C57BL, pubmed-meshheading:20228261-Muscle, Skeletal, pubmed-meshheading:20228261-Muscle Proteins, pubmed-meshheading:20228261-Proto-Oncogene Proteins c-akt, pubmed-meshheading:20228261-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20228261-SKP Cullin F-Box Protein Ligases, pubmed-meshheading:20228261-Signal Transduction, pubmed-meshheading:20228261-Ubiquitin-Protein Ligases, pubmed-meshheading:20228261-Up-Regulation
pubmed:year
2010
pubmed:articleTitle
IGF-1 prevents ANG II-induced skeletal muscle atrophy via Akt- and Foxo-dependent inhibition of the ubiquitin ligase atrogin-1 expression.
pubmed:affiliation
Heart and Vascular Institute, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural