Linked Life Data

19846573

Source:http://linkedlifedata.com/resource/pubmed/id/19846573

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-12-21
pubmed:abstractText
The mitogen-activated protein kinase (MAPK) cascade plays an important role in the regulation of various cellular functions in glomerulonephritis (GN). Here, we investigated whether extracellular signal-regulated kinase 5 (ERK5), a member of the MAPK family, is involved in the pathogenesis of chronic mesangioproliferative GN, using a rat model induced by uninephrectomy and anti-Thy-1 antibody injection. Immunostaining of kidneys obtained at different time points revealed that phospho-ERK5 was weakly expressed in control glomeruli but dramatically increased in a typical mesangial pattern after 28 and 56 days of GN. A semiquantitative assessment indicated that glomerular phospho-ERK5 expression closely paralleled the accumulation of extracellular matrix (ECM), collagen type I, as well as glomerular expression of reactive oxygen species (ROS) and ANG II. On the other hand, phospho-ERK1/2 expression increased on day 7 during the phase of enhanced mesangial cell (MC) proliferation and decreased thereafter. H(2)O(2) and ANG II each induced ERK5 phosphorylation by cultured rat MCs. Costimulation with both H(2)O(2) and ANG II synergistically increased ERK5 phosphorylation in MCs. Cultured MCs transfected with ERK5-specific small interference RNA showed a significant decrease in H(2)O(2) or ANG II-induced cell viability and soluble collagen secretion compared with control cells. Treatment of GN rats with an ANG II type 1 receptor blocker resulted in significant decreases in phospho-ERK5 expression and collagen accumulation accompanied by remarkable histological improvement. Taken together, these results suggest that MC ERK5 phosphorylation by ANG II or H(2)O(2) enhances cell viability and ECM accumulation in an experimental model of chronic GN.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1522-1466
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
298
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F167-76
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:19846573-Angiotensin II, pubmed-meshheading:19846573-Animals, pubmed-meshheading:19846573-Cell Survival, pubmed-meshheading:19846573-Cells, Cultured, pubmed-meshheading:19846573-Collagen, pubmed-meshheading:19846573-Disease Models, Animal, pubmed-meshheading:19846573-Disease Progression, pubmed-meshheading:19846573-Extracellular Matrix, pubmed-meshheading:19846573-Glomerulonephritis, pubmed-meshheading:19846573-Hydrogen Peroxide, pubmed-meshheading:19846573-Mesangial Cells, pubmed-meshheading:19846573-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:19846573-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:19846573-Mitogen-Activated Protein Kinase 7, pubmed-meshheading:19846573-Phosphorylation, pubmed-meshheading:19846573-Rats, pubmed-meshheading:19846573-Rats, Inbred Strains
pubmed:year
2010
pubmed:articleTitle
ERK5 activation enhances mesangial cell viability and collagen matrix accumulation in rat progressive glomerulonephritis.
pubmed:affiliation
Department of Pediatrics, Institute of Health Bioscience, University of Tokushima Graduate School, Tokushima, Japan. murushih@tulane.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't