ArticleRenal failure2022
Nuclear paraspeckle assembly transcript 1 promotes the podocyte injury via targeting miR-23b-3p/B-cell lymphoma-2 interacting protein 3 like axis.
Article in Renal failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors at 4 institutions in 1 country.
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Abstract
backgroundGiven the reported effects of nuclear paraspeckle assembly transcript 1 (NEAT1) on kidney injury, a study is worth formulating to investigate whether and how NEAT1 impacts podocytes. MATERIALS AND
methodsA mouse podocyte injury model was established using the adriamycin (ADR)-induced mouse podocyte cell line (MPC5). The target relationships between NEAT1 and microRNA (miR)-23b-3p and between miR-23b-3p and Bcl-2 interacting protein 3 like (BNIP3L) were verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. After ADR-induced MPC5 cells were transfected with NEAT1 overexpression plasmid (oe-NEAT1) or shNEAT1, the viability and apoptosis of MPC5 cells were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The expressions of MPC5, miR-23b-3p, BNIP3L and the factors related to podocyte injury, apoptosis and epithelial-mesenchymal transition were determined using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot.
resultsNEAT1 was high-expressed in ADR-induced cell model. After transfection with oe-NEAT1, the expression of NEAT1, the levels of marker (Desmin) and apoptosis were promoted, while the viability and the levels of podocyte injury markers (WT1, Nephrin) were inhibited in ADR-induced cells. However, shNEAT1 generated the effects opposite to oe-NEAT1. Besides, miR-23b-3p competitively bound to NEAT1 and targeted BNIP3L. MiR-23b-3p inhibitor reversed the effect of shNEAT1, while its effect could be further offset by shBNIP3L. Furthermore, miR-23b-3p inhibitor affected mouse podocyte injury through downregulating Bcl-2 and E-cadherin levels and upregulating Cleaved-caspase-3, Bax, N-cadherin, Vimentin and Snail levels, but shBNIP3L did oppositely.
conclusionNEAT1 promotes the podocyte injury
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