Source:http://linkedlifedata.com/resource/pubmed/id/17654315
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
2007-7-26
|
pubmed:abstractText |
Recent studies have suggested that carbon monoxide (CO) inhalation can reduce ischemia-reperfusion injury of kidneys. The purpose of the present study was to determine whether the direct application of CO using tricarbonylchloro (glycinato) ruthenium II (CORM3) would reduce cold-rewarm-associated apoptosis in renal tubular epithelial (RPTE) cells. RPTE cells were subjected to 48 hours of cold followed by 24 hours of rewarming with increasing concentrations (0-500 microM) of CORM3. CORM3 (100 microM) reduced apoptosis as determined by the TUNEL method from 21.6 +/- 5.2 to 5.8 +/- 1.1 % (untreated vs. treated, n = 5; p < 0.001). We subsequently observed that the incubation of RPTE cells with CORM3 induced heme oxygenase (HO)-1 gene expression. As HO-1 itself can confer protection against cold rewarm injury, we investigated the role of HO-1 in the protective actions of CORM3 using siRNA oligonucleotides directed against HO-1. CORM3 treatment of RPTE cells caused a 4.9- fold increase in HO-1 gene expression as determined by real time PCR. Prior treatment of RPTE cells with siRNAs against HO-1 was able to completely abolish the CORM3 mediated induction of HO-1 mRNA and protein. The abolition of HO-induction with siRNAs did reduce CORM3-mediated protection against cold rewarm-induced apoptosis; however, CORM3 was able to significantly protect RPTE cells against cold-rewarm injury: apoptosis was 33.7 +/- 0.9% vs. 15.4 +/- 0.5% vs. 62.8 +/- 1.5% vs. 23.5 +/- 3.4 in control cold-rewarm vs. cold-rewarm + CORM3 (100 microM) vs. cold-rewarm + HO-1 siRNA vs. cold-rewarm + CORM3 (100 microM) + HO-1 siRNA (n = 4). These results suggest that increased levels of CO alone can protect against cold-rewarm-induced apoptosis.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:issn |
0886-022X
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
29
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
543-8
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:17654315-Apoptosis,
pubmed-meshheading:17654315-Carbon Monoxide,
pubmed-meshheading:17654315-Cells, Cultured,
pubmed-meshheading:17654315-Cold Temperature,
pubmed-meshheading:17654315-Epithelial Cells,
pubmed-meshheading:17654315-Humans,
pubmed-meshheading:17654315-Kidney Tubules,
pubmed-meshheading:17654315-Organometallic Compounds,
pubmed-meshheading:17654315-Rewarming
|
pubmed:year |
2007
|
pubmed:articleTitle |
Carbon monoxide (CO) protects renal tubular epithelial cells against cold-rewarm apoptosis.
|
pubmed:affiliation |
Department of Physiology & Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA. dstec@physiology.usmed.edu
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|