Journal: Acta Pharmaceutica Sinica. B
Article Title: Hyperglycemia activates FGFR1 via TLR4/c-Src pathway to induce inflammatory cardiomyopathy in diabetes
doi: 10.1016/j.apsb.2024.01.013
Figure Lengend Snippet: Increased levels of phospho-FGFR1 in cardiomyocytes of diabetic mice. C57BL/6 mice were made diabetic by STZ. Heart tissues were harvested after 20 weeks of disease duration from diabetic (STZ) and non-diabetic control (Ctrl) mice. (A, B) Representative site-specific tyrosine kinase phosphorylation PST228 ProArray showing phosphorylated proteins (A). Magnified images and signal-to-noise ratio (SNR) of FGFR1 (Tyr766) in STZ (red box) and Ctrl (yellow box) are shown in panel (B). (C) Relative abundance of FGFR1 protein in STZ and Ctrl heart tissues from AVK276 Kinase Array were shown. (D) Representative blots showing the levels of p-FGFR1 (Tyr-766) and FGFR1 in heart tissue. GAPDH was used as a loading control. (E) Immunofluorescence staining of mouse heart tissues for p-FGFR1 (red), FGFR1 (red), and α -actinin (green). Sections were counterstained with DAPI (blue). Arrows showing p-FGFR1-positive cells (Scale bar = 50 μm). (F) Levels of p-FGFR1 (Tyr-766) and FGFR1 in primary adult mouse cardiomyocytes and cardiac fibroblasts. Cells were exposed to 33 mmol/L glucose (HG) for 15 min. GAPDH was used as loading control. (G) Levels of p-FGFR1 (Tyr-766) and FGFR1 in rat primary cardiomyocytes. Isolated cells were exposed to 33 mmol/L glucose (HG) for 15 min. GAPDH was used as loading control.
Article Snippet: Kinase Antibody Array Kit (AVK276, including 276 kinase antibodies) and Tyrosine Phosphorylation ProArray (PST228, including 228 site-specific tyrosine phosphorylation antibodies) were obtained from Full Moon Biosystems (Sunnyvale, CA USA) .
Techniques: Control, Phospho-proteomics, Immunofluorescence, Staining, Isolation