Supplementary Figure 4: Amyloid fibrils increased the HDAC2 immunosignal in the hippocampal CA1 neurons, which was attenuated by microinjection of Hdac2 siRNA.
From: Epigenetic suppression of neuroligin 1 underlies amyloid-induced memory deficiency
Amyloid fibrils increased the HDAC2 immunosignal in the hippocampal CA1 neurons, which was attenuated by microinjection of Hdac2 siRNA. Microinjection of Hdac2 siRNA (5 nmol per side), but not scrambled RNA (scRNA), significantly attenuated amyloid-upregulated Hdac2 mRNA levels (a, n = 6 rats per group, F(3,20) = 8.8, P = 0.0006) and protein (b, n = 6 rats per group, F(3,20) = 8.1, P<0.001) levels in the hippocampal CA1 area. The expression of HDAC2 was largely colocalized with the immunofluorescence signal of NeuN (c), the marker of neuron, but not GFAP (d), the marker of astrocyte. Microinjection of Hdac2 siRNA, but not scrambled RNA (scRNA), significantly attenuated the amyloid fibrils-upregulated immunofluorescence signal of HDAC2 in the hippocampal CA1 neurons (n = 24 sections from 5 rats in each group, F(3,16) = 11.5, P = 0.0003, Scale bar = 25 μm). (e) Microinjection of Hdac2 siRNA also significantly attenuated amyloid-decreased synapse number in the hippocampal CA1 area. Total synapse density was calculated as the number of synapses per 100 μm2 of neuropil (n = 5 rats per group, F(3,16) = 12.77, P = 0.0002, scale bar = 0.5 μm). Data represent mean ± s.e.m. *, P<0.05, **, P<0.01. Full length blots are presented in supplementary figure 11.
