Fig. 2: Senescent cell clearance decreases MMT. | Cell Death & Disease

Fig. 2: Senescent cell clearance decreases MMT.

From: Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease

Fig. 2

Triple-immunofluorescence images (A) and quantification (B) identified MMT cells in RAS kidneys that co-express macrophage (F4/80, red), senescence activation (p16-GFP, green), and myofibroblast (α-SMA, pink) markers, compared to controls (Normal). These MMT cell populations were significantly reduced in RAS kidneys treated with the p16INK-4a+ cell apoptosis inducer, AP20187 (RAS + AP20187). A positive correlation was observed between MMT cell populations and the number of α-SMA+ cells (D). The senescence marker SA-β-gal activity, which was elevated in RAS compared to normal kidneys, showed a significant reduction following AP20187 treatment (A, C). Scale bar: 20 µm (immunofluorescence), 50 µm (SA-β-gal). E, F The numbers of F4/80+ macrophages correlated positively with the numbers of p16INK-4a+ and SA-β-gal+ cells in both normal and RAS kidneys. G, H Similarly, renal fibrosis correlated strongly with the numbers of p16INK-4a+ and SA-β-gal+ cells in the mouse kidneys. Data are mean ± SD (n = 6 per group). *P < 0.05 vs. Normal; #P < 0.05 vs. RAS. p16-GFP: p16INK-4a+ labeled by green fluorescent protein (GFP).

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