| http://purl.uniprot.org/citations/31211440 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31211440 | http://www.w3.org/2000/01/rdf-schema#comment | "Vascular endothelial growth factor C (VEGF-C) is an angiogenic and lymphangiogenic growth factor. Recent research has revealed the role for VEGF-C in regulating autophagy by interacting with a nontyrosine kinase receptor, neuropilin-2 (NRP-2). However, whether VEGF-C participates in regulating cell survival and autophagy in renal proximal tubular cells is unknown. To address this question, we employed a cell modal of serum deprivation to verify the role of VEGF-C and its receptor NRP-2 in regulating cell survival and autophagy in NRK52E cell lines. The results show that VEGF-C rescued the loss of cell viability induced by serum deprivation in a concentration-dependent manner. Furthermore, endogenous VEGF-C was knocked down in NRK52E cells by using specific small-interfering RNAs (siRNA), cells were more sensitive to serum deprivation-induced cell death. A similar increase in cell death rate was observed following NRP-2 depletion in serum-starved NRK52E cells. Autophagy activity in serum-starved NRK52E cells was confirmed by western blot analysis of microtubule-associated protein-1 chain 3 (LC3), immunofluorescence staining of endogenous LC3, and the formation of autophagosomes by electron microscopy. VEGF-C or NRP-2 depletion further increased LC3 expression induced by serum deprivation, suggesting that VEGF-C and NRP-2 were involved in controlling autophagy in NRK52E cells. We further performed autophagic flux experiments to identify that VEGF-C promotes the activation of autophagy in serum-starved NRK52E cells. Together, these results suggest for the first time that VEGF-C/NRP-2 axis promotes survival and autophagy in NRK52E cells under serum deprivation condition. SIGNIFICANCE OF THE STUDY: More researchers had focused on the regulation of autophagy in kidney disease. The effect of VEGF-C on cell death and autophagy in renal epithelial cells has not been examined. We first identified the VEGF-C as a regulator of cell survival and autophagy in NRK52E cell lines. And VEGF-C/NRP-2 may mediate autophagy by regulating the phosphorylation of 4EBP1 and P70S6K. VEGF-C treatment may be identified as a therapeutic target in renal injury repair due to its capacity to promote tubular cell survival in the future."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.org/dc/terms/identifier | "doi:10.1002/cbf.3402"xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Liang X."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Zhang Y."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Yang Q."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Zhang C."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Xu G."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/author | "Chang X."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/name | "Cell Biochem Funct"xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/pages | "290-300"xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/title | "Roles for VEGF-C/NRP-2 axis in regulating renal tubular epithelial cell survival and autophagy during serum deprivation."xsd:string |
| http://purl.uniprot.org/citations/31211440 | http://purl.uniprot.org/core/volume | "37"xsd:string |
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