Journal: Nature communications
Article Title: GDF11 slows excitatory neuronal senescence and brain ageing by repressing p21.
doi: 10.1038/s41467-023-43292-1
Figure Lengend Snippet: Fig. 7 | In vivo selective deletion of GDF11 in excitatory neurons induced their own senescence requires p21. a, b Genetic strategy for generation of p21f/f mice (a) and CaMKIIα-Cre; GDF11f/f; p21f/f mice (b) to selectively delete both GDF11 and p21 in CaMKIIα+ neurons through Cre/Loxp system. c–g Representative images (c) and quantification (d–g) of the SA-β-Gal+ cells in the cingulate cortex (c, up, and d, n = 4 per group), layers 4 and 5 (c, middle, and e GDF11f/f, n = 4; GDF11cKO, n = 3; CaMKIIα- Cre; GDF11f/f;p21f/f, n = 5), layer 6a (c middle, and f layer 6a is the deep layer cortex near the corpus callosum (CC), GDF11f/f, n = 5; GDF11cKO, n = 4; CaMKIIα-Cre; GDF11f/
Article Snippet: Using immunofluorescence of this specific anti-GDF11 antibody, mouse anti-GDF11 antibody (R&D, MAB19581), we show that in the adult brain of mouse aged 3 months (M) (Fig. 1a), GDF11 was widely expressed in neurons in the cerebral cortex (Fig. 1b) and other parts of the CNS, consistent with a previous study17.
Techniques: In Vivo