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BEI Resources
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Image Search Results
Journal: Frontiers in Cardiovascular Medicine
Article Title: Mechanical injury accentuates lipid deposition in ApoE –/– mice and advance aortic valve stenosis: A novel modified aortic valve stenosis model
doi: 10.3389/fcvm.2023.1119746
Figure Lengend Snippet: Mechanical injury and hyperlipidemia induced advanced fatty and lipoproteins deposition beneath the leaflets endothelial. (A) Representative CD31 immunostaining (green, scale bar, 20 μm) and Oil red O staining (top, scale bar, 100 μm; bottom, scale bar, 500 μm) of aortic valves 8 weeks after wire injury. Valvular lipid deposition was only observed in hypercholesterolemic mice 8 weeks after wire injury. (B) Representative images of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). (C) Quantification of the valvular lesion area (%) 8 weeks after wire injury in the indicated groups ( n = 4 per group). (D) Quantification of apoB (scale bar, 50 μm) and apoA (scale bar, 50 μm) lipoproteins in the valvular 8 weeks after wire injury in the indicated groups ( n = 4 per group). Results are mean ± SEM. Adjusted P values were provided in case of multiple groups. ns. indicates non-significant P value. ** P < 0.01 and *** P < 0.001.
Article Snippet: For immunohistochemistry, sections were incubated with antibodies against apoB (1:50 Proteintech),
Techniques: Immunostaining, Staining
Journal: Journal of Translational Medicine
Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry
doi: 10.1186/s12967-023-04723-1
Figure Lengend Snippet: Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and
Techniques: Biomarker Discovery, Immunohistochemical staining, Staining, Immunohistochemistry, Two Tailed Test
Journal: Journal of Translational Medicine
Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry
doi: 10.1186/s12967-023-04723-1
Figure Lengend Snippet: The differently expressed proteins (DEPs) that were validated using immunohistochemistry (all up regulated) (unstable/stable)
Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and
Techniques: Immunohistochemistry, Biomarker Discovery, Significance Assay
Journal: Journal of Translational Medicine
Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry
doi: 10.1186/s12967-023-04723-1
Figure Lengend Snippet: Hypothetical characterization of altered molecular mechanisms in cells in the fibrous cap and lipid core regions of unstable carotid plaques. The expression of key proteins of ferroptosis and lipid metabolism is significantly increased in patients with unstable plaques, and there are mechanisms associated with both the promotion and inhibition of iron death. This possibly indicates that cells in different regions of the plaque are regulated by key proteins of ferroptosis that subsequently lead to increased plaque instability and expansion of the necrotic core. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic; SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5 apolipoprotein A-V; CETP cholesteryl ester transfer protein; GPX4 glutathione peroxidase 4; GSH glutathione; CoQ10 coenzyme Q10; ROS reactive oxygen species; HDL high-density lipoprotein; ox-LDL oxidized low-density lipoprotein
Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and
Techniques: Expressing, Inhibition