Intracellular Kinases Mediate Increased Translation and Secretion of Netrin-1 from Renal Tubular Epithelial Cells

Hdl Handle:
http://hdl.handle.net/10675.2/762
Title:
Intracellular Kinases Mediate Increased Translation and Secretion of Netrin-1 from Renal Tubular Epithelial Cells
Authors:
Jayakumar, Calpurnia; Mohamed, Riyaz; Ranganathan, Punithavathi Vilapakkam; Ramesh, Ganesan
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.; 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.; 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.
Citation:
PLoS One. 2011 Oct 26; 6(10):e26776
Issue Date:
26-Oct-2011
URI:
http://hdl.handle.net/10675.2/762
DOI:
10.1371/journal.pone.0026776
PubMed ID:
22046354
PubMed Central ID:
PMC3202578
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Vascular Biology Center: Faculty Research and Publication

Full metadata record

DC FieldValue Language
dc.contributor.authorJayakumar, Calpurniaen_US
dc.contributor.authorMohamed, Riyazen_US
dc.contributor.authorRanganathan, Punithavathi Vilapakkamen_US
dc.contributor.authorRamesh, Ganesanen_US
dc.date.accessioned2012-10-26T20:30:40Z-
dc.date.available2012-10-26T20:30:40Z-
dc.date.issued2011-10-26en_US
dc.identifier.citationPLoS One. 2011 Oct 26; 6(10):e26776en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22046354en_US
dc.identifier.doi10.1371/journal.pone.0026776en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/762-
dc.description.abstractBackground: 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.en_US
dc.description.abstractMethods 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.en_US
dc.description.abstractConclusion: 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.en_US
dc.rightsJayakumar 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.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectComputational Biologyen_US
dc.subjectMolecular Geneticsen_US
dc.subjectGene Expressionen_US
dc.subjectGeneticsen_US
dc.subjectGene Expressionen_US
dc.subjectMolecular Cell Biologyen_US
dc.subjectCellular Typesen_US
dc.subjectEpithelial Cellsen_US
dc.subjectSignal Transductionen_US
dc.subjectSignaling Cascadesen_US
dc.subjectMAPK signaling cascadesen_US
dc.subjectCellular Stress Responsesen_US
dc.subjectGene Expressionen_US
dc.subjectMedicineen_US
dc.subjectNephrologyen_US
dc.subjectAcute Renal Failureen_US
dc.subjectChronic Kidney Diseaseen_US
dc.titleIntracellular Kinases Mediate Increased Translation and Secretion of Netrin-1 from Renal Tubular Epithelial Cellsen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3202578en_US
dc.contributor.corporatenameVascular Biology Center-
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