| http://purl.uniprot.org/citations/20740046 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20740046 | http://www.w3.org/2000/01/rdf-schema#comment | "In retina, an ischemic injury-resistant condition (ischemic tolerance) can be induced by a sub-lethal ischemic treatment (preconditioning) prior to an otherwise injurious ischemic insult. In this work, we compared retinal proteomic changes under three different ischemic conditions, as a means to identify the effector mechanisms that underlie retinal ischemic tolerance. Transient retinal ischemia was induced by elevating the intraocular pressure (IOP) in three groups of adult rats as follows: Group 1, ischemic-preconditioned, 110 mmHg for 8 minutes followed by 48 hours reperfusion; Group 2, ischemic-injured, 110 mmHg for 60 minutes followed by 24 hours reperfusion; Group 3, ischemic-tolerant, preconditioning treatment followed by another 60 minutes of 110 mmHg and 24 hours reperfusion. Protein quantities in each of the afore-mentioned retinal ischemic conditions, as determined by quantitative mass spectrometry, were compared with that of the contralateral control eyes (sham-treated). As a result, a total of 328 proteins were identified and quantified; among them, 30-60% of proteins showed a change in abundance under one or more retinal ischemic conditions. In particular, in ischemic-tolerant retinas, histone proteins H2B, H3 and H4 demonstrated an increase in abundance, whereas histone H2A showed a decrease in abundance. Further immunohistochemical analyses confirmed the results of proteomic analyses, and detected an up regulation of tri-methylated histone H3, mono-ubiquitinated histone H2A and Polycomb group protein RING2. Together, these results suggest a role of epigenetic regulation in the induction of retinal ischemic tolerance that involves histone and polycomb proteins."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Zhou A."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Arbogast B."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Burgoyne C.F."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Lan J.Q."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Cioffi G.A."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/author | "Stowell C."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/name | "Int J Physiol Pathophysiol Pharmacol"xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/pages | "148-160"xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/title | "Retinal proteomic changes under different ischemic conditions - implication of an epigenetic regulatory mechanism."xsd:string |
| http://purl.uniprot.org/citations/20740046 | http://purl.uniprot.org/core/volume | "2"xsd:string |
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