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Results: 4

1.
Fig. 3.

Fig. 3. From: PKC? increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice.

Overexpression of PKCε does not change levels of αAPPs and C-terminal fragments (CTFs) of APP. (A Upper) A representative immunoblot of sAPP and flAPP immunoreactivity from hippocampi of individual mice. (A Lower) The quantification of immunoreactive bands, indicating no difference between the genotypes (n = 7 for APPInd and n = 8 for APPInd/PKCεTg1) in relative sAPP levels, which were normalized to the level of flAPP. (B Upper) Representative immunoblots of CTF-α (C83) and CTF-β (C99) immunoreactivity. (B Lower) No difference in levels of these CTFs between APPInd and APPInd/PKCεTg1 mice (n = 5 for each genotype). CTF immunoreactivity was normalized to GAPDH immunoreactivity.

Doo-Sup Choi, et al. Proc Natl Acad Sci U S A. 2006 May 23;103(21):8215-8220.
2.
Fig. 2.

Fig. 2. From: PKC? increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice.

PKCε decreases plaque-associated neuropathology. (A and B) Patches of GFAP-positive astrocytes were detected by confocal microscopy in the parietal cortex in singly transgenic APPInd mice but not in doubly transgenic APPInd/PKCεTg1 mice. (C and D) Dual-channel immunofluorescence images (anti-APP, green; GFAP, red) show astrocytosis and disruption of the pyramidal cell layer in the hippocampus of an APPInd mouse and no such changes in an APPInd/PKCεTg1 mouse. (E and F) Dual-channel immunofluorescence images (anti-APP, green; MAP-2, red) demonstrating plaques (arrows) and displacement of dendrites in the CA1 region of an APPInd mouse but not in an APPInd/PKCεTg1 mouse. (Scale bars: AD, 100 μm; E and F, 50 μm.)

Doo-Sup Choi, et al. Proc Natl Acad Sci U S A. 2006 May 23;103(21):8215-8220.
3.
Fig. 4.

Fig. 4. From: PKC? increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice.

Effect of PKCε on Aβ-degrading enzymes. (A and B) IDE (A) and NEP (B) activity in the forebrain were similar in APPInd mice (n = 3) and APPInd/PKCεTg1 mice (n = 5). (C and D) ECE activity in the parietal cortex (C) and hippocampus (D) of APPInd mice (n = 7) and APPInd/PKCεTg1 mice (n = 8). (E) PKCε levels were determined by Western blot analysis (Left) and ECE (Right) activity in PKCε-transfected (n = 12) and mock-transfected EA.hy926 cultures (n = 12) after treatment with 16 nM phorbol 12-myristate 13-acetate for 24 h. ∗, P < 0.05 by two-tailed, unpaired t tests in CE.

Doo-Sup Choi, et al. Proc Natl Acad Sci U S A. 2006 May 23;103(21):8215-8220.
4.
Fig. 1.

Fig. 1. From: PKC? increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice.

Overexpression of PKCε reduces amyloid plaque burden and inhibits Aβ accumulation in brain parenchyma. (A) Schematic of the human PKCε transgene. (B) Immunoblot of brain homogenates from wild-type mice (Wt) and from transgenic PKCε (Tg1 and Tg2) and nontransgenic (Ct1 and Ct2) littermates. (C) Similar distribution of PKCε-like immunoreactivity in hippocampal CA3 and CA1 regions and frontal cortex (Ctx) of Wt and PKCεTg1 mice. (D and E) Thioflavin-S staining (D) and anti-Aβ immunostaining (3D6 antibody) (E) showing fewer plaques and Aβ immunoreactive deposits in the hippocampus and neocortex in APPInd/PKCεTg1 mice than in APPInd mice. (Scale bars: 200 μm.) (F and G) Quantification of Thioflavin-S staining (F) and Aβ deposits (G) is expressed as the percentage of total surface area of the hippocampus and cortex in each section. Data are from 10 mice per genotype, averaged from three sections per mouse. ∗, P < 0.05 by two-tailed t tests.

Doo-Sup Choi, et al. Proc Natl Acad Sci U S A. 2006 May 23;103(21):8215-8220.

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