Journal: American Journal of Translational Research

Article Title: Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells

doi:

Figure Lengend Snippet: Increased activation of HSCs in Lyn TG mice upon CCl4 treatment. A: Representative immunofluorescence photomicrographs of HSC activation marker (Αvβ3, α-SMA and desmin) expression in liver tissues from WT mice and Lyn TG mice after administration of CCl4 (×200 magnification). B: The fluorescence intensity of desmin in 8 random fields. C: The fluorescence intensity of α-SMA in 8 random fields. D: The fluorescence intensity of Αvβ3 in 8 random fields. E: TGF-β1 levels in the liver tissues were determined by ELISA. All of the data are presented as the mean ± s.d. One-way ANOVA (Tukey-Kramer post-test) was used for Statistical analysis.

Article Snippet: After blocking with 1% BSA (Sigma-Aldrich) containing 0.05% Tween 20 for 1 hour, the specimens were then incubated with anti-Lyn antibody (Santa Cruz, CA, sc-15, AB_2281450), anti-integrin αvβ3 antibody (Bioss, China, bs-1310R), anti-α-SMA antibody (Bioss, China, bs-0189R), anti-desmin antibody (Bioss, China, bs-1026R), and anti-COL1α1 antibody (Bioss, China, bs-10423R).

Techniques: Activation Assay, Immunofluorescence, Marker, Expressing, Fluorescence, Enzyme-linked Immunosorbent Assay

Journal: American Journal of Translational Research

Article Title: Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells

doi:

Figure Lengend Snippet: Lyn kinase increased the activation of HSCs in vitro. Immunohistochemical staining for HSC activation marker (Αvβ3, α-SMA and COL1α1) expression in TGF-β1-induced LX-2 and Lyn+/+ LX-2. A: Representative photomicrographs and fluorescence intensity of α-SMA in cells (×400 magnification). B: Representative photomicrographs and fluorescence intensity of Αvβ3 in cells (×400 magnification). C: Representative photomicrographs and fluorescence intensity of COL1α1 in cells (×400 magnification). All of the data are presented as the mean ± s.d. One-way ANOVA (Tukey-Kramer post-test) was used for Statistical analysis. LX-2 cell lines transfected with lentiviral vector expressing Lyn were described as Lyn+/+ cells. LX-2 cell lines transfected with control lentiviral vector were described as WT cells.

Article Snippet: After blocking with 1% BSA (Sigma-Aldrich) containing 0.05% Tween 20 for 1 hour, the specimens were then incubated with anti-Lyn antibody (Santa Cruz, CA, sc-15, AB_2281450), anti-integrin αvβ3 antibody (Bioss, China, bs-1310R), anti-α-SMA antibody (Bioss, China, bs-0189R), anti-desmin antibody (Bioss, China, bs-1026R), and anti-COL1α1 antibody (Bioss, China, bs-10423R).

Techniques: Activation Assay, In Vitro, Immunohistochemical staining, Staining, Marker, Expressing, Fluorescence, Transfection, Plasmid Preparation

Journal: American Journal of Translational Research

Article Title: Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells

doi:

Figure Lengend Snippet: The Src-specific inhibitor PP2 suppressed HSC activation. A: Immunohistochemical staining for HSC activation marker (Αvβ3) expression in TGF-β1-induced LX-2 and Lyn+/+ LX-2 in the presence of PP2 (×400 magnification). The fluorescence intensity of Αvβ3 in cells was measured. B: Apoptotic cells of LX-2 were detected by flow cytometry. All of the data are presented as the mean ± s.d. One-way ANOVA (Tukey-Kramer post-test) was used for Statistical analysis.

Article Snippet: After blocking with 1% BSA (Sigma-Aldrich) containing 0.05% Tween 20 for 1 hour, the specimens were then incubated with anti-Lyn antibody (Santa Cruz, CA, sc-15, AB_2281450), anti-integrin αvβ3 antibody (Bioss, China, bs-1310R), anti-α-SMA antibody (Bioss, China, bs-0189R), anti-desmin antibody (Bioss, China, bs-1026R), and anti-COL1α1 antibody (Bioss, China, bs-10423R).

Techniques: Activation Assay, Immunohistochemical staining, Staining, Marker, Expressing, Fluorescence, Flow Cytometry

Journal: Biomaterials Research

Article Title: Bifunctional Tumor-Targeted Bioprobe for Phothotheranosis

doi: 10.34133/bmr.0002

Figure Lengend Snippet: In vivo evaluation of tumor targetability and biodistribution of cRGD-ZW800-PEG. cRGD-ZW800-PEG (500 nmol) was injected into a murine xenograft model of HNSCC. (A) Quantitative time-course assessment up to 24 h postinjection ( n = 7, mean ± SEM; ** P < 0.01, **** P < 0.0001). Scale bars = 5 mm. (B) Biodistribution and SBR of resected organs and tumors. SBR was determined by comparing the signals of major organs against muscle ( n = 3, mean ± SEM). Scale bar = 5 mm. Ga, gallbladder; He, heart; Lu, lungs; Li, liver; Pa, pancreas; Sp, spleen; Ki, kidneys; Du, duodenum; In, intestine; Mu, muscle; Ga, gallbladder; Bl, bladder; Tu, tumor. (C) Histological and (D) immunohistochemical analyses of integrin αvβ3 in the tumor. The tumor was sectioned 4 h postinjection, imaged on the fluorescence microscopy, and then stained with an anti-αvβ3 antibody, followed by an appropriate secondary antibody using avidin-biotin complex/diaminobenzidine histochemistry. Scale bar = 200 μm. (E) Immunofluorescence staining of integrin αvβ3 and CD31 in the tumor. Tumors were excised when the tumor volume reached around 80 mm 3 and stained with anti-αvβ3 and anti-CD31 antibodies, followed by appropriate secondary antibodies. Scale bar = 50 μm.

Article Snippet: The following antibody was used to visualize integrin αvβ3: Integrin Alpha V + Beta 3 polyclonal antibody (50-198-2620; Fisher Scientific, 1:200).

Techniques: In Vivo, Injection, Immunohistochemical staining, Fluorescence, Microscopy, Staining, Avidin-Biotin Assay, Immunofluorescence