Linked Life Data

14975939

Source:http://linkedlifedata.com/resource/pubmed/id/14975939

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-6-21
pubmed:abstractText
Mechanical strain affects airway myocyte phenotype, cytoskeletal architecture, proliferation, and contractile function. We hypothesized that (i) short-term mechanical strain modulates transcription of smooth muscle-specific gene promoters for SM22 and smooth muscle myosin heavy chain (smMHC); and (ii) strain-induced change is mediated by altered actin polymerization in association with activation of protein kinase C (PKC). Primary cultured canine tracheal myocytes were transiently transfected with luciferase reporter plasmids harboring a murine SM22, human smMHC, or artificial serum response factor (SRF)-specific gene promoter and then subjected to cyclic strain for 48 h. This strain protocol significantly reduced transcriptional activity of SM22 and smMHC promoters and an artificial SRF-dependent promoter by 55 +/- 5.9%, 57 +/- 6.4%, and 75 +/- 7.9%, respectively, with concomitant reduction in F/G actin ratio by 31 +/- 8%. PKC inhibitors, GF109203X or Gö6976, significantly attenuated these affects. Similar to strain, strain-independent activation of PKC inhibited SM22, smMHC, and SRF-dependent promoter activity by 61 +/- 4%, 66 +/- 5%, and 28 +/- 15%, respectively, and reduced the F/G actin ratio by 30 +/- 5%. Gel shift assay revealed that PKC activation led to decreased binding of the required transcription factor, SRF, to CArG elements in the SM22 promoter. These data suggest a previously unknown role for PKC isoforms in mechanosensitive signaling in airway myocytes that is associated with coordinated regulation of actin cytoskeletal dynamics and smooth muscle-specific gene transcription.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-61
pubmed:dateRevised
2011-11-10
pubmed:meshHeading
pubmed-meshheading:14975939-Actins, pubmed-meshheading:14975939-Animals, pubmed-meshheading:14975939-Bronchi, pubmed-meshheading:14975939-Cell Differentiation, pubmed-meshheading:14975939-Cells, Cultured, pubmed-meshheading:14975939-Dogs, pubmed-meshheading:14975939-Down-Regulation, pubmed-meshheading:14975939-Enzyme Inhibitors, pubmed-meshheading:14975939-Gene Expression Regulation, Developmental, pubmed-meshheading:14975939-Genes, Regulator, pubmed-meshheading:14975939-Microfilament Proteins, pubmed-meshheading:14975939-Muscle Proteins, pubmed-meshheading:14975939-Myocytes, Smooth Muscle, pubmed-meshheading:14975939-Myosin Heavy Chains, pubmed-meshheading:14975939-Promoter Regions, Genetic, pubmed-meshheading:14975939-Protein Kinase C, pubmed-meshheading:14975939-Respiration, pubmed-meshheading:14975939-Serum Response Factor, pubmed-meshheading:14975939-Stress, Mechanical, pubmed-meshheading:14975939-Transfection
pubmed:year
2004
pubmed:articleTitle
Mechanical strain inhibits airway smooth muscle gene transcription via protein kinase C signaling.
pubmed:affiliation
Department of Psysiology, University of Manitoba, Winnipeg, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't