Linked Life Data

20067797

Source:http://linkedlifedata.com/resource/pubmed/id/20067797

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-2-15
pubmed:abstractText
Deposition of collagen IV in proximal tubule cells (PTCs) plays an important role during diabetic nephropathy, but the mechanism underlying excessive production of collagen IV remains poorly understood. In this study, we examined the miRNA profile of HK-2 cells and found that high glucose/TGF-beta1 induced significant down-regulation of miR-29a. We then showed that miR-29a negatively regulated collagen IV by directly targeting the 3'UTRs of col4a1 and col4a2. These results suggest that miR-29a acts as a repressor to fine-tune collagen expression and that the reduction of miR-29a caused by high glucose may increase the risk of excess collagen deposition in PTCs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1873-3468
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
584
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
811-6
pubmed:dateRevised
2010-5-20
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
High glucose down-regulates miR-29a to increase collagen IV production in HK-2 cells.
pubmed:affiliation
Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't