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Results: 6

1.
Fig. 1.

Fig. 1. From: Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

CD36 deletion in 3-, 18-, and 22-mo-old Tg2576 mice improves attenuation in the increased CBF produced by neural activity (whisker stimulation) (A), endothelium-dependent vasodilator acetylcholine (B), hypercapnia (C), and smooth muscle relaxant adenosine (D) (n = 5/group). The attenuation in the CBF responses induced by aging in CD36wt/wt littermates is also ameliorated by CD36 deletion. *P < 0.05 from 3 mo; #P < 0.05 from CD36wt/wt, ANOVA and Tukey test.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2013 February 19;110(8):3089-3094.
2.
Fig. 2.

Fig. 2. From: Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

CD36 deletion attenuates Aβ1-40, but not Aβ1-42 or plaque load, in 18-mo-old Tg2576 mice. (A and B) SDS-soluble Aβ1-40 (A) and FA-soluble (SDS-insoluble) Aβ1-40 (B) are reduced in Tg2576/CD360/0 mice (n = 5/group; P < 0.05). (C–F) The distribution of amyloid plaques, assessed using 4G8 immunocytochemistry (C and D), and the number per square millimeter (E) and percent occupied area (F) do not differ between Tg2576/CD36wt/wt and Tg2576/CD360/0 mice (n = 5/group; P > 0.05).

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2013 February 19;110(8):3089-3094.
3.
Fig. 5.

Fig. 5. From: Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

CD36 deletion rescues the reduced LRP-1 and ZO-1 in the somatosensory cortex of Tg2576 mice. LRP-1 (A–C) and ZO-1 (D–F) immunofluorescence in WT (CD36wt/wt), Tg2576 (Tg2576/CD36wt/wt), and Tg2576 mice lacking CD36 (Tg2576/CD360/0). (G–I) Quantification of LRP-1, ZO-1, and number of microvessels, identified by the endothelial marker CD31. Microvascular expression of LRP-1 (A, B, and G, n = 5/group; P < 0.05) and ZO-1 (D, E, and H, n = 5/group; P < 0.05) is suppressed in Tg2576 mice, an effect rescued by CD36 deletion (C, F, G, and H; P > 0.05 from CD36wt/wt). (I) The number of cortical microvessels does not differ between groups (n = 5/group; P > 0.05).

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2013 February 19;110(8):3089-3094.
4.
Fig. 6.

Fig. 6. From: Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

CD36 deletion ameliorates cognitive function in Tg2576 mice assessed using the Y maze (n = 10/group). (A–C) The reductions in novel arm entry (A), time spent in the novel arm (B), and arm alternation (C) observed in Tg2576/CD36wt/wt mice are partially rescued by CD36 deletion. (D) The number of arm visits is increased in Tg2576/CD36wt/wt mice, reflecting hyperactivity, an effect also attenuated by CD36 deletion. *P < 0.05 from CD36wt/wt; #P < 0.05 from 3 mo, χ2 test in A, ANOVA and Tukey test in B–D.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2013 February 19;110(8):3089-3094.
5.
Fig. 4.

Fig. 4. From: Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

CD36 deletion rescues the alterations in pericytes in Tg2576 mice. Pericytes, identified by PDGFR-β immunostaining, and microvessels, identified by the basement membrane marker Col IV, in 18-mo-old CD36wt/wt (A–E), Tg2576/CD36wt/wt (F–J), and Tg2576/CD360/0 (K–O) mice. (G and P) In Tg2576/CD36wt/wt mice (n = 5/group), pericyte cell bodies are reduced in number (P), but their processes are hypertrophic and envelop the capillaries outlining their contours (G). (J and Q) On EM, the vascular basal lamina is thickened and the pericyte processes are more extensive (J), such that the area of the vessel covered by processes is increased (n = 130–143 vessels from 3 mice/group) (Q). These alterations are ameliorated in Tg2576 mice lacking CD36 in K–Q (P < 0.05 from CD36wt/wt).

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2013 February 19;110(8):3089-3094.
6.
Fig. 3.

Fig. 3. From: Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

CD36 deletion selectively attenuates CAA and reduces smooth muscle cell fragmentation in 18- and 22-mo-old Tg2576 mice. Confocal images illustrate thioflavin-S+ vessels, identified by double-labeling with the smooth muscle marker α-actin in the somatosensory cortex. (A–C) Dense amyloid deposits are seen in pial and penetrating arterioles (arrows) in Tg2576 mice. (D–F) CAA load is attenuated in Tg2576 mice lacking CD36. (G–J) Smooth muscle cells are fragmented in Tg2576 mice compared with WT mice (G and H, arrowheads), which is attenuated by CD36 deletion (I and J). (K) CAA burden, expressed as percent of α-actin+ vessels that also display thioflavin-S, is attenuated in Tg2576 mice lacking CD36 (n = 5/group). *P < 0.05 from Tg2576/CD36wt/wt. (L) The number of smooth muscle cell fragments, reflecting smooth muscle damage and expressed as fragmentation index (SI Materials and Methods), is normalized in Tg2576 mice lacking CD36 at age 18 mo and reduced in these mice at age 22 mo (n = 40–60 arterioles/group). *P < 0.05 from CD36wt/wt; #P < 0.05 from Tg2576/CD36wt/wt.

Laibaik Park, et al. Proc Natl Acad Sci U S A. 2013 February 19;110(8):3089-3094.

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