Intracellular Kinases Mediate Increased Translation and Secretion of Netrin-1 from Renal Tubular Epithelial Cells
dc.contributor.author | Jayakumar, Calpurnia | |
dc.contributor.author | Mohamed, Riyaz | |
dc.contributor.author | Ranganathan, Punithavathi Vilapakkam | |
dc.contributor.author | Ramesh, Ganesan | |
dc.date.accessioned | 2012-10-26T20:30:40Z | |
dc.date.available | 2012-10-26T20:30:40Z | |
dc.date.issued | 2011-10-26 | en_US |
dc.identifier.citation | PLoS One. 2011 Oct 26; 6(10):e26776 | en_US |
dc.identifier.issn | 1932-6203 | en_US |
dc.identifier.pmid | 22046354 | en_US |
dc.identifier.doi | 10.1371/journal.pone.0026776 | en_US |
dc.identifier.uri | http://hdl.handle.net/10675.2/762 | |
dc.description.abstract | Background: Netrin-1 is a laminin-related secreted protein, is highly induced after tissue injury, and may serve as a marker of injury. However, the regulation of netrin-1 production is not unknown. Current study was carried out in mouse and mouse kidney cell line (TKPTS) to determine the signaling pathways that regulate netrin-1 production in response to injury. | |
dc.description.abstract | Methods and Principal Findings: Ischemia reperfusion injury of the kidney was induced in mice by clamping renal pedicle for 30 minutes. Cellular stress was induced in mouse proximal tubular epithelial cell line by treating with pervanadate, cisplatin, lipopolysaccharide, glucose or hypoxia followed by reoxygenation. Netrin-1 expression was quantified by real time RT-PCR and protein production was quantified using an ELISA kit. Cellular stress induced a large increase in netrin-1 production without increase in transcription of netrin-1 gene. Mitogen activated protein kinase, ERK mediates the drug induced netrin-1 mRNA translation increase without altering mRNA stability. | |
dc.description.abstract | Conclusion: Our results suggest that netrin-1 expression is suppressed at the translational level and MAPK activation leads to rapid translation of netrin-1 mRNA in the kidney tubular epithelial cells. | |
dc.rights | Jayakumar et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | en_US |
dc.subject | Research Article | en_US |
dc.subject | Biology | en_US |
dc.subject | Computational Biology | en_US |
dc.subject | Molecular Genetics | en_US |
dc.subject | Gene Expression | en_US |
dc.subject | Genetics | en_US |
dc.subject | Gene Expression | en_US |
dc.subject | Molecular Cell Biology | en_US |
dc.subject | Cellular Types | en_US |
dc.subject | Epithelial Cells | en_US |
dc.subject | Signal Transduction | en_US |
dc.subject | Signaling Cascades | en_US |
dc.subject | MAPK signaling cascades | en_US |
dc.subject | Cellular Stress Responses | en_US |
dc.subject | Gene Expression | en_US |
dc.subject | Medicine | en_US |
dc.subject | Nephrology | en_US |
dc.subject | Acute Renal Failure | en_US |
dc.subject | Chronic Kidney Disease | en_US |
dc.title | Intracellular Kinases Mediate Increased Translation and Secretion of Netrin-1 from Renal Tubular Epithelial Cells | en_US |
dc.type | Article | en_US |
dc.identifier.pmcid | PMC3202578 | en_US |
dc.contributor.corporatename | Vascular Biology Center | |
refterms.dateFOA | 2019-04-10T00:48:14Z | |
html.description.abstract | Background: Netrin-1 is a laminin-related secreted protein, is highly induced after tissue injury, and may serve as a marker of injury. However, the regulation of netrin-1 production is not unknown. Current study was carried out in mouse and mouse kidney cell line (TKPTS) to determine the signaling pathways that regulate netrin-1 production in response to injury. | |
html.description.abstract | Methods and Principal Findings: Ischemia reperfusion injury of the kidney was induced in mice by clamping renal pedicle for 30 minutes. Cellular stress was induced in mouse proximal tubular epithelial cell line by treating with pervanadate, cisplatin, lipopolysaccharide, glucose or hypoxia followed by reoxygenation. Netrin-1 expression was quantified by real time RT-PCR and protein production was quantified using an ELISA kit. Cellular stress induced a large increase in netrin-1 production without increase in transcription of netrin-1 gene. Mitogen activated protein kinase, ERK mediates the drug induced netrin-1 mRNA translation increase without altering mRNA stability. | |
html.description.abstract | Conclusion: Our results suggest that netrin-1 expression is suppressed at the translational level and MAPK activation leads to rapid translation of netrin-1 mRNA in the kidney tubular epithelial cells. |