Comparison of the major membrane glycoproteins and proteins of human, rabbit and rat blood platelets

Toor, Bina; McGregor, John L.; McGregor, Lilian; Clemetson, Kenneth J.

doi:10.1016/0049-3848(82)90250-x

Cited by 12 publications

(4 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although the rat platelet receptor for GspB is unknown, these cells are also extensively glycosylated [30], suggesting that sialyl T-antigen or a similar carbohydrate moiety may also serve as the binding site for this adhesin.…”

Section: Discussionmentioning

confidence: 99%

Role of the serine-rich surface glycoprotein GspB of Streptococcus gordonii in the pathogenesis of infective endocarditis

Xiong

Bensing

Bayer

et al. 2008

Microbial Pathogenesis

118

View full text Add to dashboard Cite

The direct binding of bacteria to platelets is a central interaction in the pathogenesis of infective endocarditis. GspB is a serine-rich, cell wall glycoprotein of Streptococcus gordonii that mediates the binding of this organism to human platelets in vitro. To assess the contribution of this adhesin to the pathogenesis of endocarditis, we compared the virulence of S. gordonii M99 (which expresses GspB) with an isogenic, gspB mutant (PS846) in two rat models of endovascular infection. In the first group of experiments, animals were infected intravenously with M99 or PS846, and sacrificed 72 h later, to assess levels of bacteria within cardiac vegetations, kidneys, and spleens. When inoculated with 105 CFU, rats infected with PS846 had significantly lower densities of organisms within vegetations (mean: 3.84 log10 CFU/g) as compared with M99-infected rats (6.67 log10 CFU/g; P < 0.001). Marked differences were also seen in rats co-infected with M99 and PS846, at a 1:1 ratio. While M99 was found at high levels within vegetations, kidneys and spleens (mean log10 CFU/g: 6.62, 5.07 and 4.18, respectively) PS846 was not detected within these tissues. Thus, platelet binding by GspB appears to be a major interaction in the pathogenesis of endocarditis due to S. gordonii.

show abstract

Section: Discussionmentioning

confidence: 99%

Role of the serine-rich surface glycoprotein GspB of Streptococcus gordonii in the pathogenesis of infective endocarditis

Xiong

Bensing

Bayer

et al. 2008

Microbial Pathogenesis

118

View full text Add to dashboard Cite

show abstract

“…Independent groups of investigators, on the other hand, working with rabbits and rhesus monkeys [ 1-51, have presented evidence indicating that in these animals, platelets decrease in buoyant density with age. Many structural, kinetic, biochemical, and functional aspects of platelet biology differ among mammals-ie, blood platelet number, size, mean survival time [25], response to aggregating agents [25,26], platelet surface proteins and glycoproteins [25,27], dense body number and compo-sition [28,29], activity of the arachidonate pathway [25,30,31], etc. The possibility that intrinsic differences among species could explain part of the conflicting results reported on the relationship between platelet age and density prompted us to investigate this problem in mongrel dogs.…”

Section: Discussionmentioning

confidence: 99%

Kinetics of platelet density subpopulations in splenectomized mongrel dogs

et al. 1984

View full text Add to dashboard Cite

Autologous 51Cr-platelet kinetic studies were performed in splenectomized mongrel dogs. Mean survival time of PRP-platelets was 5.4 +/- 1.5 (SD) days (n = 6). The curves, though slightly curvilinear, showed mostly a linear type of decay, denoting that platelet removal from the circulation is mainly determined by aging of the cells. High-density (HD) and low-density (LD) platelet cohorts were isolated in Stractan gradients from samples drawn daily after infusion of labeled platelets. Specific radioactivity in HD cohorts declined rapidly postinfusion (T1/2 = 1.3 days), but specific radioactivity in LD platelets increased for 2 days and steadily declined for 4 days thereafter (n = 6). Labeled HD platelets, comprising 11.7% of the total population, lived significantly longer in circulation than LD platelets (19.1% of the total population) (n = 3). The patterns of decay of the radioactivity, however, do not have all the characteristics of pure age-cohort survival curves; 3.7 days after the infusion of labeled HD platelets, the specific radioactivity in LD cohorts was six times higher than on day 1, but attained only 20% of the initial specific radioactivity in HD platelets. After the infusion of labeled LD platelets no radioactivity was recovered in circulating HD cohorts. These findings indicate that mongrel dog platelets decrease in density with aging, but also that platelet density heterogeneity is in part determined during the thrombopoietic process. These data are consistent with those of other authors in rabbits and rhesus monkeys, but contrast with the observations that platelets in humans, baboons, and Macaca fascicularis monkeys increase in density with age, suggesting that the displacement of platelets toward compartments of either higher or lower density depends on the species under study.

show abstract

“…Extensive study has been carried out with murine platelets to investigate the biology of human platelets due to the similarity between rat and human platelets [ 61 , 62 ]. However, rat platelets showed a distinct response to human platelets in a number of cases, raising concerns about using rat platelets instead of human platelets [ 63 , 64 ]. Therefore, the procoagulant effects of PHMG-p on platelets should be confirmed with human platelets in further research.…”

Section: Discussionmentioning

confidence: 99%

Polyhexamethylene Guanidine Phosphate Enhanced Procoagulant Activity through Oxidative-Stress-Mediated Phosphatidylserine Exposure in Platelets

Choi,

Kim

2024

Toxics

View full text Add to dashboard Cite

Polyhexamethylene guanidine phosphate (PHMG-p) is a common biocidal disinfectant that is widely used in industry and household products. However, PHMG-p was misused as a humidifier disinfectant (HD) in South Korea, which had fatal health effects. Various health problems including cardiovascular diseases were observed in HD-exposed groups. However, the potential underlying mechanism of HD-associated cardiovascular diseases is poorly understood. Here, we examined the procoagulant activity of platelets caused by PHMG-p and clarified the underlying mechanism. PHMG-p enhanced phosphatidylserine (PS) exposure through alteration of phospholipid transporters, scramblase, and flippase. Intracellular calcium elevation, intracellular ATP depletion, and caspase-3 activation appeared to underlie phospholipid transporter dysregulation caused by PHMG-p, which was mediated by oxidative stress and mitochondrial dysfunction. Notably, antioxidant enzyme catalase and calcium chelator EGTA reversed PHMG-p-induced PS exposure and thrombin generation, confirming the contributive role of oxidative stress and intracellular calcium in the procoagulant effects of PHMG-p. These series of events led to procoagulant activation of platelets, which was revealed as enhanced thrombin generation. Collectively, PHMG-p triggered procoagulant activation of platelets, which may promote prothrombotic risks and cardiovascular diseases. These findings improve our understanding of HD-associated cardiovascular diseases.

show abstract

Comparison of the major membrane glycoproteins and proteins of human, rabbit and rat blood platelets

Cited by 12 publications

References 24 publications

Role of the serine-rich surface glycoprotein GspB of Streptococcus gordonii in the pathogenesis of infective endocarditis

Role of the serine-rich surface glycoprotein GspB of Streptococcus gordonii in the pathogenesis of infective endocarditis

Kinetics of platelet density subpopulations in splenectomized mongrel dogs

Polyhexamethylene Guanidine Phosphate Enhanced Procoagulant Activity through Oxidative-Stress-Mediated Phosphatidylserine Exposure in Platelets

Contact Info

Product

Resources

About