文章基本信息

标题：Author Correction: Angiotensin II induces kidney inflammatory injury and fibrosis through binding to myeloid differentiation protein-2 (MD2)
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作者：Zheng Xu ; Weixin Li ; Jibo Han 等
期刊名称：Scientific Reports
电子版ISSN：2045-2322
出版年度：2021
卷号：11
DOI：10.1038/s41598-021-94987-8
语种：English
出版社：Springer Nature
摘要：Correction to: Scientific Reports https://doi.org/10.1038/srep44911, published online 21 March 2017 This Article contains errors in Figures 1 and 3. In Figure 1D, the TEM images of the KO group and the AngII + KO group are incorrect. In Figure 3A, the GAPDH blot is a duplication of the GAPDH blot in Figure 3C. Additionally, in Figure 3C, the IκB and the Lamin B blots are incorrect. The correct Figures 1 and 3 and accompanying legends appear below. Figure 1 MD2 −/− mice were protected from Ang II-induced renal dysfunction and tissue remodeling. WT and MD2 −/− (KO) mice were injected subcutaneously with 1.4 mg·kg −1·day Ang II for 8 weeks, and blood and tissue samples were collected for analysis (Methods). Ctrl = vehicle injection in WT mice, Ang II = Ang II injecton in WT mice, KO = vehicle injection in MD2 −/− mice, Ang II + KO = Ang II injection in MD2 −/− mice; 8 mice/group. Kidney function indices, ( A) serum creatinine level, ( B) serum albumin/serum creatinine ratio and ( C) blood urea nitrogen (BUN) in mmol/L. ( D) Top row shows representative histological image kidney tissue from 5 mice per group (hematoxylin and eosin, 400× magnification); bottom row shows representative images from transmission electron microscopic (TEM) evaluation of renal tissue from each experimental group; 20,000× magnification. ( E) Representative Western blot analysis of kidney tissue for marker proteins of tissue modeling (Col = collagen, TGF-β = transforming growth factor β, and MMP-9 = matrix metalloproteinase 9; GAPDH as loading control; the densitometric quantification was shown in Supplementary Figure S1. The gels were run under the same experimental conditions. Shown are cropped gels/blots (The gels/blots with indicated cropping lines are shown in Supplementary Figure S6). ( F) Representative histochemical images for renal tissue fibrosis from 5 mice per group evaluated by Masson’s trichrome staining (blue), Sirius red staining (red), and collagen 1 immunochemistry (Col-1)(brown); 400× magnification. ( G) The mRNA expression of the TGF-β, Col1, Col4 and MMP-9 in renal tissue was determined by real-time qPCR; values were normalized to housekeeping gene β-actin. For data in ( A, B, G), values are reported as mean ± S.E.M from 8 mice per group; #P < 0.05 versus Ctrl; *P < 0.05, **P < 0.01 versus Ang II-treated group). Figure 3 L6H21 pretreatment prevents Ang II-induced fibrosis and signal activation in renal tubular epithelial cells. The effects of the MD2 inhibitor L6H21 on Ang II-stimulated inflammatory responses in the renal tubular epithelial cell line, NRK-52E, were determined. NRK-52E were pretreated with the vehicle control DMSO (Ctrl) or L6H21 (2.5, 5.0, 10 μM) for 1 h, and stimulated with Ang II (1 μM) for different periods. ( A) Representative Western blot analysis for protein markers of fibrosis, Col-1 (collagen 1), Col-4 (collagen 4), MMP-9 (metalloproteinase 9), and TGF-β (transforming growth factor β), GAPDH as loading control; n = 3 independent determinations. ( B) The mRNA levels of TGF-β, Col-1 (collagen 1), Col-4, CTGF, and MMP-9 were detected by real-time qPCR; values normalized to house-keeping gene β-actin. ( C) Representative Western blot analysis for p-ERK (phosphorylated ERK) and IκB from total cell lysate, GAPDH as loading addingol, ERK = total ERK; NF-κB p65 subunit detected from nuclear cell fraction, lamin B as loading control; n = 3 independent determinations. ( D) The mRNA levels of IL-1β, IL-6 and TNF-α were detected by real-time qPCR; values normalized to house-keeping gene β-actin. ( E) Representative immunofluorescent distribution of NF-κB p65 subunit (Texas-red streptavidin), top row; same cells counterstained with nuclear stain DAPI, bottom row, 200× magnification; n = 3 independent determinations. Data in B and D are reported as mean ± S.E.M. of n = 3, *P < 0.05, **P < 0.01, ***P < 0.001 versus Ang II-treated group; #P < 0.05 and ##P < 0.01 versus Ctrl. For panels ( A, C) the gels were run under the same experimental conditions. Shown are cropped gels/blots (The gels/blots with indicated cropping lines are shown in Supplementary Figure S6).