Extended Data Fig. 8: Immunohistochemistry analysis of microglia activation and proteinase-K resistant α-synuclein aggregates in mice with Tet2 inactivation 11 months after exposure to inflammation.
From: Epigenomic analysis of Parkinson’s disease neurons identifies Tet2 loss as neuroprotective
Immunohistochemistry image analysis of microglial activation in the (a) dorsal striatum and the (b) substantia nigra. Representative images of dorsal striatum and substantia nigra microglia (IBA1-positive). n = 9 wild-type + saline, 10 wild-type + LPS, 14 Tet2 knockout + saline, and 10 Tet2 knockout + LPS. Immunohistochemistry image analysis of proteinase-K resistant α-synuclein aggregates in the (c) dorsal striatum and the (d) substantia nigra. Data analyzed by two-way ANOVA followed by post hoc Tukey HSD test. n = 9 wild-type + saline, 9 wild-type + LPS, 14 Tet2 knockout + saline, and 7 Tet2 knockout + LPS. Error bars represent s.e.m. e, Transcript analysis of inflammatory marker genes in the midbrain of wild-type and Tet2 knockout mice 11 months post-LPS or saline injection. Transcript levels of IL-1β, IL-6, NFKB2, RELA and TNF-α were analyzed by qPCR and normalized to housekeeping genes HPRT and GAPDH. n = 6 wild-type + saline, 8 wild-type + LPS, 5 Tet2 knockout + saline, 10 Tet2 knockout + LPS. f, Tet2 inactivation does not induce differences in midbrain Tet1 or Tet3 transcript levels. Tet1 and Tet3 transcript levels in the midbrain of wild-type (Tet2+/+) and Tet2 knockout (Tet2-/-) mice 24 h after saline or LPS treatment (n = 4 wild-type + saline, 4 wild-type + LPS, 3 Tet2 knockout + saline, 3 Tet2 knockout + LPS). There was no significant change in Tet1 or Tet3 expression between mouse groups, as determined by a generalized linear model. Transcript levels in counts per million (cpm) from RNA-seq data. e, f, Boxplot center line is the mean, the bounds of the box are the lower and upper quartiles, and the whiskers extend to minimum and maximum data points within 1.5 times the interquartile range.
