Fig 2: miR-26a KO aggravates Ang-II infusion-induced kidney damage. (A) 24-h urinary protein quantity at the 4th week post Ang-II infusion in WT and miR-26a KO mice (n = 6). (B) SCr levels at the 4th week of Ang-II infusion in WT and miR-26a-KO mice (n = 6). (C) Representative Western blot figure showing the levels of IL-1β, IL-18, α-SMA, and FN in the kidney of mice. (D) Semi-quantitative statistical analysis of IL-1β, IL-18, α-SMA, and FN protein levels by Western blotting test (n = 6). (E) Representative immunofluorescence staining of CD68 (green) in kidney. Scale bars: 40 μm. (F) Representative Masson’s staining of kidney. Scale bars: 20 μm. Data are presented as mean ± SD. Ang: Angiotensin; CD: Cluster of differentiation; Ctrl: Control; DAPI: 4′,6-diamidino-2-phenylindole; FN: Fibronectin; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; IL: Interleukin; KO: Knockout; miR: MicroRNA; SCr: Serum creatinine; SD: Standard deviation; WT: Wild type; α-SMA: α-smooth muscle actin.

Fig 3: Overexpression of miR-26a significantly improved Ang-II-induced cardiorenal injury. (A) Semi-quantitative statistical analysis of LIMS1, ILK, IL-1β, IL-18, α-SMA and FN protein levels in heart for Western blotting results (n = 6). (B) Representative Masson’s staining of heart and kidney. Scale bars: 20 μm. (C) Representative immunofluorescence staining of CD68 (green) in heart and kidney. Scale bars: 40 μm. (D) Semi-quantitative statistical analysis of LIMS1, ILK, IL-1β, IL-18, α-SMA and FN protein levels in kidney for Western blotting results (n = 6). Data are presented as mean ± SD. Ang: Angiotensin; CD: Cluster of differentiation; Ctrl: Control; DAPI: 4′,6-diamidino-2-phenylindole; FN: Fibronectin; IL: Interleukin; ILK: Integrin-linked kinase; KO: Knockout; LIMS: LIM and senescent cell antigen-like domain 1; miR: MicroRNA; SCr: Serum creatinine; SD: Standard deviation; α-SMA: α-smooth muscle actin.

Fig 4: Inhibition of LIMS1 significantly improved Ang-II-induced kidney injury. (A) Semi-quantitative statistical analysis of LIMS1, ILK, IL-1β, IL-18, α-SMA and FN protein levels in kidney for Western blotting results (n = 6). (B) 24-h urinary protein quantity at the 4th week of Ang-II infusion in WT and miR-26a-KO mice (n = 6). (C) SCr levels at the 4th week of Ang-II infusion in WT and miR-26a KO mice (n = 6). (D) Representative immunofluorescence staining of CD68 (green) in kidney. Scale bars: 40 μm. (E) Representative Masson’s staining of kidney. Scale bars: 20 μm. Data are presented as mean ± SD. Ang: Angiotensin; CD: Cluster of Differentiation; Ctrl: Control; DAPI: 4′,6-diamidino-2-phenylindole; FN: Fibronectin; IL: Interleukin; ILK: Integrin-linked kinase; KO: Knockout; LIMS1: LIM and senescent cell antigen-like domain 1; miR: MicroRNA; SCr: Serum creatinine; SD: Standard deviation; WT: Wildtype; α-SMA: α-smooth muscle actin.

Fig 5: miR-26a KO aggravates Ang-II infusion-induced cardiac damage. (A) M-mode echocardiograms showing left ventricular dimensions. (B) Real-time PCR analysis of ANP, BNP, and β-MHC mRNA levels (n = 6). (C) Representative immunofluorescence staining of WGA (green) in heart. Scale bars: 40 μm. (D) Representative immunofluorescence staining of CD68 (green) in heart. Scale bars: 40 μm. (E) Representative Western blot figure showing the levels of IL-1β, IL-18, α-SMA, and FN in the heart of mice. (F) Semi-quantitative statistical analysis of IL-1β, IL-18, α-SMA, and FN protein levels for Western blotting (n = 6). (G) Representative Masson’s staining of heart. Scale bars: 20 μm. Data are presented as mean ± SD. Ang: Angiotensin; ANP: Atrial natriuretic peptide; BNP: Brain natriuretic peptide; CD: Cluster of Differentiation; Ctrl: Control; DAPI: 4′,6-diamidino-2-phenylindole; FN: Fibronectin; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; IL: Interleukin; KO: Knockout; miR: MicroRNA; PCR: Polymerase chain reaction; SD: Standard deviation; WGA: Wheat germ agglutinin; WT: Wild type; α-SMA: α-smooth muscle actin; β-MHC: β-myosin heavy chain.