Journal: Molecular Medicine Reports

Article Title: Molecular responses of radiation-induced liver damage in rats

doi: 10.3892/mmr.2014.3051

Figure Lengend Snippet: Immunohistochemical staining of liver sections 3 days and 1, 2, 4, 8 and 12 weeks after 20 Gy irradiation. Brown color denotes positivity. The perivenous area was the major area of positive staining. TGF-β1, Smad3, CTGF and NF-κB p65 staining was positive between 3 days and 12 weeks after irradiation. Smad4 and Smad7 staining was positive between 3 days and 1 week after irradiation. TNF-α staining was positive between 1 and 4 weeks after irradiation. (Magnification, ×200). Gy, grays; TGF-β1, transforming growth factor-β1; CTGF, connective tissue growth factor; TNFα, tumor necrosis factor-α, NF, nuclear factor.

Article Snippet: The primary antibodies used were as follows: Rabbit monoclonal antibodies against transforming growth factor-β1 (TGF-β1; 1:250), nuclear factor (NF)-κB65 (1:100), mothers against decapentaplegic homolog 4 (Smad4) (1:40), Smad3 (1:250), Smad7 (1:30), tumor necrosis factor-α (TNF-α; 1:200) and connective tissue growth factor (CTGF; 1:200), all purchased from Boster Co., Ltd.

Techniques: Immunohistochemical staining, Staining, Irradiation

Journal: Molecular Medicine Reports

Article Title: Molecular responses of radiation-induced liver damage in rats

doi: 10.3892/mmr.2014.3051

Figure Lengend Snippet: Western blot analysis (ratio of the molecules investigated, vs. GAPDH). Similar to the results obtained using the reverse transcription quantitative polymerase chain reaction, the protein expression levels were as follows: NF-κB p65 was increased between 3 days and 12 weeks after irradiation. CTGF and Smad3 were significantly increased between 2 and 12 weeks after irradiation. TGF-β1 was significantly increased between 1 and 12 weeks after irradiation and TNF-α was significantly increased between 3 days and 4 weeks after irradiation. Smad4 was significantly increased between 3 days and 1 week after irradiation. Smad7 was significantly increased 3 days after irradiation and reduced significantly 1 and 2 weeks after irradiation, however, it remained higher than that in the control. From 4 weeks post-irradiation, the protein expression of Smad7 returned to the control level. * P<0.05, ** P<0.001 compared with the control group (0 Gy). Gy, grays; CTGF, connective tissue growth factor; TGF-β1, transforming growth factor-β1; TNFα, tumor necrosis factor-α; Smad, mothers against decapentaplegic; NF, nuclear factor.

Article Snippet: The primary antibodies used were as follows: Rabbit monoclonal antibodies against transforming growth factor-β1 (TGF-β1; 1:250), nuclear factor (NF)-κB65 (1:100), mothers against decapentaplegic homolog 4 (Smad4) (1:40), Smad3 (1:250), Smad7 (1:30), tumor necrosis factor-α (TNF-α; 1:200) and connective tissue growth factor (CTGF; 1:200), all purchased from Boster Co., Ltd.

Techniques: Western Blot, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Irradiation, Control

Journal: Molecular Medicine Reports

Article Title: Molecular responses of radiation-induced liver damage in rats

doi: 10.3892/mmr.2014.3051

Figure Lengend Snippet: mRNA expression levels were determined using reverse transcription quantitative polymerase chain reaction (ratio of the molecules investigated, vs. GAPDH). The mRNA expression of NF-κB p65 was upregulated between 3 days and 12 weeks after irradiation. The mRNA expression levels were as follows: CTGF and Smad3 were significantly upregulated between 2 and 12 weeks after irradiation. TGF-β1 was significantly upregulated between 1 and 12 weeks after irradiation. TNF-α was significantly upregulated between 3 days and 4 weeks after irradiation. Smad4 was significantly upregulated 3 days and 1 week after irradiation. Smad7 was significantly upregulated 3 days after irradiation and reduced significantly 1–2 weeks after irradiation, however, the expression levels remained higher than that in the control. From 4 weeks post-irradiation, the mRNA expression of Smad7 returned to the control level. * P<0.05, ** P<0.001, compared with the control group (0 Gy). CTGF, connective tissue growth factor; TGF-β1, transforming growth factor-β1; TNFα, tumor necrosis factor-α, Smad, mothers against decapentaplegic; NF, nuclear factor.

Article Snippet: The primary antibodies used were as follows: Rabbit monoclonal antibodies against transforming growth factor-β1 (TGF-β1; 1:250), nuclear factor (NF)-κB65 (1:100), mothers against decapentaplegic homolog 4 (Smad4) (1:40), Smad3 (1:250), Smad7 (1:30), tumor necrosis factor-α (TNF-α; 1:200) and connective tissue growth factor (CTGF; 1:200), all purchased from Boster Co., Ltd.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Irradiation, Control

Journal: The Journal of Biological Chemistry

Article Title: Albumin-based Microbubbles Bind Up-regulated Scavenger Receptors following Vascular Injury *

doi: 10.1074/jbc.M110.134809

Figure Lengend Snippet: Immunohistochemical staining of balloon-injured and control rat aortic tissue for the presence of microbubbles (i.e. human albumin), CD36, TLR-4, and CD68. A, staining for PESDA microbubble proteins at sites of injury demonstrated microbubble retention in a focal pattern in the intimal and media of the aorta. Of note, PESDA shell proteins co-localized with CD36, SRB-1, and TLR-4 (white arrows), but not with CD68. ImageJ co-localization is also presented. B, images are enlarged to better illustrate co-localization of PESDA and TLR-4. However, note that PESDA and TLR-4 were not exclusively co-localized. ImageJ image processing was performed to determine areas of co-localization, which are presented in their respective panels as white pixels. Control tissues illustrate the basal expression of CD36 and were negative for PESDA and CD68. Isotype controls were negative for background staining. Pictures are representative of three infrarenal aortas from control animals and three balloon-injured animals. Scale bars = 50 μm.

Article Snippet: Samples were blocked using 5% donkey serum, washed, and incubated with the following combinations of primary antibodies: rabbit anti-rat CD36 (Novus Biologicals, Littleton, CO), TLR-4 (Rockland, Gilbertsville, PA), mouse anti-rat CD68 (AbD Serotec, Raleigh, NC), and goat anti-human albumin (Bethyl Laboratories, Montgomery, TX).

Techniques: Immunohistochemical staining, Staining, Expressing

Journal: The Journal of Biological Chemistry

Article Title: Albumin-based Microbubbles Bind Up-regulated Scavenger Receptors following Vascular Injury *

doi: 10.1074/jbc.M110.134809

Figure Lengend Snippet: CHO cells were incubated with PESDA only or with PESDA after pretreatment of the CHO cells with the oxidized ligands ox-LDL and MAA-LDL. Pretreatment with these oxidized proteins completely inhibited the binding of PESDA to SRB-1. Note that despite significant inhibition of binding to CD36, SRA, TLR-2, and TLR-4, inhibition was not complete and variable when comparing different receptors and inhibitors. *, p ≤ 0.01 compared with CHO-K1 cell binding; #, p ≤ 0.01 compared PESDA binding to each individual CHO cell expressing the scavenger receptor. Data are expressed as the mean ± S.E. of three separate experiments.

Article Snippet: Samples were blocked using 5% donkey serum, washed, and incubated with the following combinations of primary antibodies: rabbit anti-rat CD36 (Novus Biologicals, Littleton, CO), TLR-4 (Rockland, Gilbertsville, PA), mouse anti-rat CD68 (AbD Serotec, Raleigh, NC), and goat anti-human albumin (Bethyl Laboratories, Montgomery, TX).

Techniques: Incubation, Binding Assay, Inhibition, Expressing