Linked Life Data

15353229

Source:http://linkedlifedata.com/resource/pubmed/id/15353229

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2004-9-8
pubmed:abstractText
The Akt serine/threonine kinase mediates pro-survival signalings in retina and was reported to be activated in a response to some retinal and optic nerve injuries. Human and experimental glaucoma induce apoptosis of retinal ganglion cells (RGCs). The purpose of this study is to test whether episcleral vein cauterization (EVC) to chronically elevate intraocular pressures (IOPs) in rats increase apoptosis of RGCs and affect activation of Akt and its upstream insulin-like growth factor (IGF)-1 receptor/Insulin receptor. Three episcleral veins in left eyes of Sprague-Dawley rats were cauterized to elevate IOPs. Up to 6 months, IOPs were monitored and the retina was dissected at several time points. The numbers of terminal dUTP nick end labeling (TUNEL)-positive cells and those of RGCs labeled with fluorogold were counted in flat-mounted retina. Immunohistochemistry and immunoblotting were performed to identify cells expressing phosphorylated Akt and to quantify the phospho- to total ratios of Akt and IGF-1 receptor/insulin receptor. EVC significantly elevated IOPs up to 2 months, increased TUNEL-positive cells in an IOP-dependent fashion, and reduced 34.5% of RGCs at 6 months (P<0.001) compared with contralateral retinas. Phosphorylated Akt was specifically expressed in RGCs until 1 month after cauterization. Akt (P=0.036) and IGF-1 receptor/Insulin receptor (P=0.003) were transiently phosphorylated at 3 days. Intrinsic activation of the IGF-1 receptor/Insulin receptor to Akt pathway may occur in RGCs in retina with EVC.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
1022
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
195-204
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15353229-Animals, pubmed-meshheading:15353229-Antigens, CD11b, pubmed-meshheading:15353229-Blotting, Western, pubmed-meshheading:15353229-Burns, Electric, pubmed-meshheading:15353229-Cell Death, pubmed-meshheading:15353229-Disease Models, Animal, pubmed-meshheading:15353229-Enzyme Activation, pubmed-meshheading:15353229-Functional Laterality, pubmed-meshheading:15353229-Glaucoma, pubmed-meshheading:15353229-Glial Fibrillary Acidic Protein, pubmed-meshheading:15353229-Immunohistochemistry, pubmed-meshheading:15353229-In Situ Nick-End Labeling, pubmed-meshheading:15353229-Insulin, pubmed-meshheading:15353229-Intraocular Pressure, pubmed-meshheading:15353229-Male, pubmed-meshheading:15353229-Microtubule-Associated Proteins, pubmed-meshheading:15353229-Phosphorylation, pubmed-meshheading:15353229-Proto-Oncogene Proteins c-akt, pubmed-meshheading:15353229-Rats, pubmed-meshheading:15353229-Rats, Sprague-Dawley, pubmed-meshheading:15353229-Receptor, IGF Type 1, pubmed-meshheading:15353229-Retina, pubmed-meshheading:15353229-Retinal Ganglion Cells, pubmed-meshheading:15353229-Sclera, pubmed-meshheading:15353229-Stilbamidines, pubmed-meshheading:15353229-Time Factors, pubmed-meshheading:15353229-Veins
pubmed:year
2004
pubmed:articleTitle
Akt is activated via insulin/IGF-1 receptor in rat retina with episcleral vein cauterization.
pubmed:affiliation
Department of Organ Therapeutics, Division of Ophthalmology, Kobe University Graduate School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't