Fig 2: Proposed mechanism of HDL mediated cardiac protection in SHR. Chronic, in vivo treatment with HDL reduced blood pressure and protected SHR against myocardial I/R injury. HDL induced cardiac protection required SR-BI and involved attenuation of autophagy and inflammation. Created with Biorender.com.

Fig 3: Cardiac SR-BI Expression in WKY and SHR. Total heart homogenates (A) and membrane preparations (B) from WKY and SHR and total heart homogenates from WKY and SHR implanted with vehicle or HDL containing osmotic pumps (C) were subjected to immunoblotting against SR-BI and GAPDH as a loading control. Data are expressed as means ± SEM, *P < 0.05, n = 5–6 rats per group.

Fig 4: P. berghei sporozoites can infect primary mouse hepatocytes through CD81-and SR-B1-independent pathways. (A) Primary hepatocytes isolated from WT or SR-B1 deficient C57BL/6 mice were infected with PbGFP sporozoites in the absence or presence of neutralizing anti-mCD81 mAb MT81, and cultured for 24 h before EEF quantification (mean control values for each experiment without MT81: 63 and 266 EEFs/well in srb1+/+ hepatocytes; 94, 311 and 420 EEFs/well in srb1-/- hepatocytes). *p < 0.05 (ratio paired t test). (B)P. berghei infection in Hepa1-6 cells was inhibited by the anti-mCD81 mAb MT81 antibody (mean control values for each experiment without MT81: 0.64 and 1.09% PbGFP-infected cells).

Fig 5: Schematic of the mechanisms by which HDL is hypothesized to protect cerebrovascular functions in AD. a In the absence of HDL, when Aß peptides enter the vessel wall they are either taken up by SMC via LRP1 (1a) or become trapped in ECM, particularly when enriched in collagen-I (1b). 2) Accumulation of Aß in the vessel wall induces endothelial activation and subsequent binding and transmigration of blood-derived circulating monocytes. 3) Astrocytes on the antelumen of penetrating arteries secret apoE that reduces collagen-I levels in the vascular wall. b in the presence of HDL, 4) HDL reduces monocyte binding via SR-BI (4a), whereas reduction of CAA is independent of SR-BI (4b). 5) HDL enters the cerebrovascular wall through undefined mechanisms and reduce Aß uptake by SMC maybe by reducing LRP1 levels (5a), bind and remodel collagen-I fibres via HDL-apoE particles (5b) and form a complex with Aß (5c), all of which increase luminal recovery of Aß. 6) The reduction of CAA is specific to HDL