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Authors: Baker, Richard F. | Clark, Linda J.

Article Type: Research Article

Abstract: Treatment of intact fresh human red cells with phosphate and calcium ions, in that order, led to cell agglutination at room temperature, and hemolysis and fusion at 37°C within 30–60 minutes. During incubation, cell-associated calcium increased 70 fold, while ATP levels declined by 98%. Agglutination was much reduced after neuraminidase treatment, suggesting that surface negative charges play a role in phosphate-calcium bridging between cells. Incorporation of 10 mM EGTA into resealed ghosts increased the fusion index relative to control ghosts while the incorporation of 1 mM calcium had the opposite effect. Aggregation of membrane-associated proteins was demonstrated by freeze-fracture and …by glycoprotein labeling. In summary, phosphate and calcium ions cause agglutination of red cells and an increased permeability to cations resulting in hemolysis, an aggregation of membrane proteins and finally fusion of adjacent protein-free lipid bilayers. Show more

Keywords: human red cells, fusion, ATP, phosphate, calcium, agglutination

DOI: 10.3233/BIR-1979-164-502

Citation: Biorheology, vol. 16, no. 4-5, pp. 285-292, 1979

Authors: Rhodin, Johannes A. | Thomas, Tom N. | Clark, Linda | Garces, Amanda | Bryant, Margaret

Article Type: Research Article

Abstract: Vascular dysfunction and inflammatory processes may be early events in the pathology of Alzheimer's disease (AD). Even though amyloid β-peptides (Aβ) play a prominent role in the initiation and progression of cellular dysfunction in AD, the precise in vivo actions of various Aβ-peptides has not been established. The cerebrovascular actions of the major Aβ-peptides (1–40) and (1–42) in live animals were investigated using an open cranial window technique. We show here that the Aβ-peptides cause vascular lesions, especially in the arterioles. In one set of experiments, leukocytes and platelets were tagged with Rhodamine 6G, soluble Aβ(1–40) infused intravenously for 2 …minutes, and the vasculature video recorded for 90 minutes. In a second set of experiments, soluble Aβ(1–40) infusion was followed 30 minutes later by an infusion of soluble Aβ(1–42) and the vasculature recorded for 90 minutes. Fluorescent and transmission electron microscopic examinations demonstrated the following cerebrovascular action of Aβ-peptides: endothelial cell damage, leukocyte adhesion, platelet activation, thrombus formation, impeded blood flow, and smooth muscle cell damage. The vascular disruption observed were similar to those observed in the brains of some AD patients and may represent the initial phase of a vascular inflammatory response associated with cerebral amyloid angiopathy. The combination of Aβ(1–40) and (1–42) produced significantly more vascular disruption than Aβ(1–40) alone. Oral administration of conjugated estrogens in ovariectomized female rats protected them from the deleterious actions of Aβ-peptides. The reported protective effect of estrogen against AD may be mediated in part through prevention of cerebrovascular Aβ toxicity. Show more

Keywords: Alzheimer's disease, amyloid β-proteins, inflammation, leukocyte-platelet-endothelial interaction, thrombosis, conjugated estrogens, cranial window technique

DOI: 10.3233/JAD-2003-5403

Citation: Journal of Alzheimer's Disease, vol. 5, no. 4, pp. 275-286, 2003