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).
