Fig. 3. Astrocyte-specific or forebrain neuronal specific Tgfb1 gene deletion in the Aldh1l1^CreER or Camk2a^CreER drivers does not affect the homeostasis of microglia or GFAP expression in astrocytes in adult mouse brain (cortex).

A Astrocyte iKO mouse model and experimental timeline. B, C Representative immunohistochemistry images of cortex from TAM treated (8 weeks post) control B Aldh1l1^CreERTgfb1^wt/wt and C iKO Aldh1l1^CreER Tgfb1^fl/fl tissue showing IBA1, TMEM119, P2RY12, CD68, and GFAP immunostaining. Quantification of microglia ramification via D process terminal end numbers, E total process length, and F % of CD68+ immunoreactive area. G Quantification of astrocyte reactivity using GFAP immunoreactive positive area fraction, quantification of H TMEM119, and I P2RY12 immunoreactivity. (D, E, G, n = 5 control, n = 4 iKO) and (F, H, I, n = 3 control and n = 3, 4, and 5 for iKO). J Neuronal iKO mouse model and experimental timeline. K, L Representative images of TAM treated (8 weeks post) control Camk2a^CreERTgfb1^wt/wt (K) and iKO Camk2^CreER Tgfb1^fl/fl (L) tissue showing IBA1, TMEM119, P2RY12, CD68, and GFAP immunoreactivity. Quantification of microglia ramification via M process terminal end number, N total process length, and O CD68+ immunoreactive % area. P Quantification of astrocyte reactivity using GFAP+ immunoreactive area fraction, and quantification of Q TMEM119 and R P2RY12 immunoreactivity (M, N, P, n = 5 control and n = 4 iKO) and (O, Q, R, n = 3 for both control and iKO). Mean ± SE (>40 microglia were quantified for each animal and the average from one mouse was plotted as a single data point in the figure panel and treated as n = 1 for statistical analysis). ns = not significant. Two-sided Student’s t-test, scale bar = 100 µm. A, J Created with BioRender.com and released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license. Source data are provided as a source data file.