Results

RDF/XMLNTriplesTurtleShow queryShare ▶
SubjectPredicateObject
http://purl.uniprot.org/citations/25929436http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25929436http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Augmenter of liver regeneration (ALR) is a growth factor that is ubiquitously expressed in multiple forms among eukaryotes. The present study focused on the role of endogenous ALR on the hypoxia/reoxygenation (H/R)-induced inflammatory response in human kidney 2 (HK-2) cells, and the underlying molecular mechanisms.

Methods

To determine the relationship between exogenous and endogenous ALR, exogenous ALR was administrated to HK-2 cells, and endogenous ALR protein and mRNA expression was examined by Western blotting and quantitative real-time polymerase chain reaction (qPCR), respectively. In order to knockdown endogenous ALR expression, HK-2 cells were infected with lentiviral shRNA/ALR, after which cell viability was determined by the MTS cell viability assay. Cells were subjected to hypoxia for 6 h and reoxygenation for 12 h. Levels of monocyte chemotactic protein (MCP-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA) and qPCR. Cells were harvested, and nuclear and phosphorylated protein extracts were prepared from the HK-2 cell lysates. Nuclear factor κB (NF-κB), and phosphorylated extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) were analyzed by Western blotting. The translocation of NF-κB was detected by immunofluorescence.

Results

Exogenous ALR inhibited the expression of endogenous ALR. Lentiviral shRNA/ALR markedly downregulated endogenous ALR expression, whereas there were no changes in ALR expression in lentiviral shRNA/control HK-2 cells. The results of the MTS assay showed that silencing ALR expression did not influence cell viability. H/R led to increased production of MCP-1, IL-6, and TNF-α. However, knockdown of ALR attenuated the inflammatory response via inhibition of ERK, p38, and JNK phosphorylation. The translocation of NF-κB into the nucleus was also decreased.

Conclusions

These results suggest that there is a negative feedback loop involving ALR in HK-2 cells. Knockdown of ALR exerts anti-inflammatory actions via suppression of the mitogen-activated protein kinase signaling pathway."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.org/dc/terms/identifier"doi:10.1007/s00011-015-0825-x"xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/author"Guo H."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/author"Sun H."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/author"Xia N."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/author"Yan R."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/name"Inflamm Res"xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/pages"453-462"xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/title"Knockdown of augmenter of liver regeneration in HK-2 cells inhibits inflammation response via the mitogen-activated protein kinase signaling pathway."xsd:string
http://purl.uniprot.org/citations/25929436http://purl.uniprot.org/core/volume"64"xsd:string
http://purl.uniprot.org/citations/25929436http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25929436
http://purl.uniprot.org/citations/25929436http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25929436
http://purl.uniprot.org/uniprot/#_H3BQQ4-mappedCitation-25929436http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/#_P55789-mappedCitation-25929436http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/#_Q9H2X5-mappedCitation-25929436http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/#_Q9NY86-mappedCitation-25929436http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/#_Q9UQK8-mappedCitation-25929436http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/H3BQQ4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/Q9H2X5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/Q9UQK8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25929436
http://purl.uniprot.org/uniprot/P55789http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25929436
▶