Comparative hemostatic parameters in BALB/c, C57BL/6 and C3H/He mice

Barrios, Margenny; Rodrı́guez-Acosta, Alexis; Gil, Amparo; Salazar, Ana Marı́a; Taylor, Peter; Sánchez, Elda E.; Arocha-Piñango, Carmen Luisa; Guerrero, Belsy

doi:10.1016/j.thromres.2008.11.001

Cited by 32 publications

(26 citation statements)

References 38 publications

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“…BALB/c females that received 1000 mg/kg, the highest AAs dose, showed slightly decreased levels of hematocrit and hemoglobin compared to the Ctrl and CNO groups. Hemoglobin values in all female study groups are consistent with those reported by Barrios et al (2009) andTsai et al (2002) in control mice. The hematocrit values obtained in the present study were lower than those described by other authors (Nemzek et al, 2001;Mazzaccara et al, 2008); however, when compared with values in the Reference Guide of the Animal Facility of the São Paulo Medical School at the University of São Paulo (2000), hematocrit values for the female A1000 mg/kg group were still within the local reference ranges (33.2 ± 3.8 animal facility vs. 34.34 ± 1.68 A1000).…”

Section: Discussionsupporting

confidence: 87%

Acute, subacute toxicity and mutagenic effects of anacardic acids from cashew (Anacardium occidentale Linn.) in mice

Carvalho

Annoni

Silva

et al. 2011

Journal of Ethnopharmacology

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Section: Discussionsupporting

confidence: 87%

Acute, subacute toxicity and mutagenic effects of anacardic acids from cashew (Anacardium occidentale Linn.) in mice

Carvalho

Annoni

Silva

et al. 2011

Journal of Ethnopharmacology

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“…Their numbers were manually calculated and summarized in all photomicrographs, and the platelet/erythrocyte ratio was then calculated. Based on the literature, in non-thrombocytopenic mice the platelet/erythrocyte ratio is 12.3 × 10 5 /9.23 × 10 6 = 0.13 ≈ 0.1 [30, 44]. …”

Section: Methodsmentioning

confidence: 99%

“…Together, these explanations create the impression that the release of Aβ by platelets occurs at very low concentrations. On the other hand, platelets are the second most common cell in the blood after erythrocytes (about 1 per 10 erythrocytes in mouse blood, [30]). We suggest that during thrombosis, especially in the chronic process accompanied by clot formation and an increase in platelet concentration, Aβ peptide released by blood platelets or cleaved from released APP is an additional source of Aβ in the brain in many cases of AD.…”

Section: Introductionmentioning

confidence: 99%

Platelets are responsible for the accumulation of β-amyloid in blood clots inside and around blood vessels in mouse brain after thrombosis

Kucheryavykh

Dávila-Rodríguez

Rivera-Aponte

et al. 2017

Brain Research Bulletin

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Introduction Platelets contain beta-amyloid precursor protein (APP) as well as Aβ peptide (Aβ) that can be released upon activation. During thrombosis, platelets are concentrated in clots and activated. Methods We used in vivo fluorescent analysis and electron microscopy in mice to determine to what degree platelets are concentrated in clots. We used immunostaining to visualize Aβ after photothrombosis in mouse brains. Results Both in vivo results and electron microscopy revealed that platelets were 300–500 times more concentrated in clots than in non-clotted blood. After thrombosis in control mice, but not in thrombocytopenic animals, Aβ immunofluorescence was present inside blood vessels in the visual cortex and around capillaries in the entorhinal cortex. Conclusion The increased concentration of platelets allows enhanced release of Aβ during thrombosis, suggesting an additional source of Aβ in the brains of Alzheimer’s patients that may arise if frequent micro-thrombosis events occur in their brains.

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“…Plasma plasmin activity was determined after treatment with human uPA [26]. Plasma samples (2 μl; n = 10 for each group) were acidified with 0.1 N HCl (10 μl) and 0.38% sodium citrate (3 μl), and incubated for 1 hour at room temperature to denature plasma proteins and to make Plg more effectively activated by uPA.…”

Section: Methodsmentioning

confidence: 99%

Plasminogen Tochigi mice exhibit phenotypes similar to wild-type mice under experimental thrombotic conditions

Tashima¹,

Banno²,

Kita³

et al. 2017

PLoS ONE

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Plasminogen (Plg) is a precursor of plasmin that degrades fibrin. A race-specific A620T mutation in Plg, also known as Plg-Tochigi, originally identified in a patient with recurrent venous thromboembolism, causes dysplasminogenemia with reduced plasmin activity. The Plg-A620T mutation is present in 3–4% of individuals in East Asian populations, and as many as 50,000 Japanese are estimated to be homozygous for the mutant 620T allele. In the present study, to understand the changes of thrombotic phenotypes in individuals with the mutant 620T allele, we generated knock-in mice carrying the homozygous Plg-A622T mutation (PlgT/T), an equivalent to the A620T mutation in human Plg. PlgT/T mice grew normally but showed severely reduced plasmin activity activated by urokinase, equivalent to ~8% of that in wild-type mice. In vitro fibrin clot lysis in plasma was significantly slower in PlgT/T mice than in wild-type mice. However, all experimental models of electrolytic deep vein thrombosis, tissue factor-induced pulmonary embolism, transient focal brain ischaemic stroke, or skin-wound healing showed largely similar phenotypes between PlgT/T mice and wild-type mice. Protein S-K196E mutation (Pros1E/E) is a race-specific genetic risk factor for venous thromboembolism. Coexistence in mice of PlgT/T and Pros1E/E did not affect pulmonary embolism symptoms, compared with those in Pros1E/E mice. Hence, the present study showed that the Plg-A622T mutation, which confers ~8% plasmin activity, does not increase the risk of thrombotic diseases in mice under experimental thrombotic conditions and does not modify the thrombotic phenotype observed in Pros1E/E mice. PlgT/T mice can be used to investigate the potential pathophysiological impact of the Plg-A620T mutation.

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Comparative hemostatic parameters in BALB/c, C57BL/6 and C3H/He mice

Cited by 32 publications

References 38 publications

Acute, subacute toxicity and mutagenic effects of anacardic acids from cashew (Anacardium occidentale Linn.) in mice

Acute, subacute toxicity and mutagenic effects of anacardic acids from cashew (Anacardium occidentale Linn.) in mice

Platelets are responsible for the accumulation of β-amyloid in blood clots inside and around blood vessels in mouse brain after thrombosis

Plasminogen Tochigi mice exhibit phenotypes similar to wild-type mice under experimental thrombotic conditions

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