Blood Clotting Activation During Normal Pregnancy

Comeglio, Paolo; Fedi, Sandra; Liotta, Agatina Alessandrello; Cellai, Anna Paola; Chiarantini, E; Prisco, Domenico; Mecacci, Federico; Parretti, Elena; Mello, Giorgio; Abbate, Rosanna

doi:10.1016/0049-3848(96)00176-4

Cited by 65 publications

(29 citation statements)

References 9 publications

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“…We next asked whether the effect of Aβ [25][26][27][28][29][30][31][32][33][34][35] on RBCs, the other abundant cell ADP induced robust platelet aggregation under similar experimental conditions as expected. As Aβ has lately been shown to interact with fibrinogen (27), we subsequently studied the effect of fibrinogen added at physiological concentrations (36) to washed platelets in the presence of Aβ. Fibrinogen (2 mg/mL) significantly impaired platelet aggregation (p < 0.0001; tracing 3, Figure 1B), ATP release (p = 0.0021; tracing 3′, Figure 1B) and P-selectin exposure (p = 0.047; Figure 1E) induced by Aβ [25][26][27][28][29][30][31][32][33][34][35] (20 μmol/L), while addition of BSA at similar concentrations to platelet suspension had no effect (tracings 4 and 4', Figure 1B).…”

Section: Fibrinogen Prevents Interaction Of Aa With Platelets and Neumentioning

confidence: 99%

Plasma Fibrinogen Is a Natural Deterrent to Amyloid β-Induced Platelet Activation and Neuronal Toxicity

Sonkar

Kulkarni

Chaurasia

et al. 2016

Mol Med

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Alzheimer's disease (AD) is a devastating neurodegenerative disorder, characterized by extensive loss of neurons and deposition of amyloid β (Aβ) in the form of extracellular plaques. Aβ is considered to have a critical role in synaptic loss and neuronal death underlying cognitive decline. Platelets contribute to 95% of circulating amyloid precursor protein that releases Aβ into circulation. We have recently demonstrated that the Aβ active fragment containing amino acid sequence 25-35 (Aβ [25][26][27][28][29][30][31][32][33][34][35] ) is highly thrombogenic in nature and elicits strong aggregation of washed human platelets in a RhoA-dependent manner. In this study, we evaluated the influence of fibrinogen on Aβ-induced platelet activation. Intriguingly, Aβ failed to induce aggregation of platelets suspended in plasma but not in buffer. Fibrinogen brought about dose-dependent decline in aggregatory response of washed human platelets elicited by Aβ [25][26][27][28][29][30][31][32][33][34][35] , which could be reversed by increasing doses of Aβ. Fibrinogen also attenuated Aβ-induced platelet responses such as secretion, clot retraction, rise in cytosolic Ca +2 and reactive oxygen species. Fibrinogen prevented intracellular accumulation of full-length Aβ peptide (Aβ 42 ) in platelets as well as neuronal cells. We conclude that fibrinogen serves as a physiological check against the adverse effects of Aβ by preventing its interaction with cells. online address: http://www.molmed.org

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Section: Fibrinogen Prevents Interaction Of Aa With Platelets and Neumentioning

confidence: 99%

Plasma Fibrinogen Is a Natural Deterrent to Amyloid β-Induced Platelet Activation and Neuronal Toxicity

Sonkar

Kulkarni

Chaurasia

et al. 2016

Mol Med

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“…Moreover, pregnancy is characterized by the enhancement of the innate immune system and suppression of the adaptive immune response [24]. Accumulating evidence in support of this view includes: 1) an increased number of granulocytes in maternal blood [25]; 2) phenotypic and metabolic changes in granulocytes and monocytes (increased expression of adhesion molecules, baseline intracellular reactive oxygen, and oxidative burst) [26,27]; 3) an increased concentration of acute phase proteins (fibrinogen, clotting factors, globulin) [28,29]; and 4) a shift of the T helper-1 to T helper-2 cell cytokine profile [30,31].…”

Section: Introductionmentioning

confidence: 99%

Normal pregnancy is characterized by systemic activation of the complement system

Richani

Soto

Romero

et al. 2005

The Journal of Maternal-Fetal & Neonatal Medicine

174

123

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Background. The complement system, a major component of innate immunity, has recently been implicated in the mechanisms of fetal loss and placental inflammation in the anti-phospholipid antibody syndrome. Inhibition of complement has been proposed as an absolute requirement for normal pregnancy. Yet, pregnancy is characterized by a generalized activation of the innate immune system. This study was conducted to determine whether or not normal pregnancy is associated with complement activation in the maternal circulation. Methods. Anaphylatoxins (C3a, C4a and C5a) were determined in the plasma of normal pregnant (20-42 wks; n = 134) and non-pregnant women (n = 40). These complement split products (C3a, C4a and C5a) were measured using specific immunoassays. Non-parametric statistics were used for analysis. Results. 1) The median plasma concentrations of C3a, C4a and C5a were significantly higher in normal pregnant women than in non-pregnant women (all p 5 0.001); 2) the concentration of C3a, C4a and C5a did not change with gestational age (p 4 0.05); and 3) the median plasma concentration of C3a had a positive correlation with the plasma C4a and C5a concentrations (r = 0.36, p 5 0.001 and r = 0.35, p 5 0.001, respectively). Conclusion. 1) Normal human pregnancy is associated with evidence of complement activation, as determined by higher concentrations of the anaphylatoxins C3a, C4a and C5a in the maternal circulation; and 2) we propose that physiologic activation of the complement system during pregnancy is a compensatory mechanism aimed at protecting the host against infection.

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“…Evidence supporting of this view includes: (1) the total white blood cell count in maternal blood increases with advancing gestational age [40]; (2) there is an increased concentration of acute phase proteins, such as fibrinogen and clotting factors [41,42]; (3) the complement system is activated in normal pregnancy [43,44]; (4) leukocytes from normal pregnant women have phenotypic and metabolic changes of monocytes and granulocytes, that are consistent with either priming or activation of the cells [2,45,46]; (5) impaired neutrophil apoptosis [47]; and (6) in the course of conducting longitudinal studies, the laboratory of Luppi et al at the University of Pittsburgh has demonstrated that monocytes during pregnancy have higher production of interleukin (IL)-12 and IL-1β compared to those in non-pregnant women [48]. Similar results were reported by Sacks et al [49] in a cross-sectional study.…”

Section: Intravascular Inflammation: a Physiologic Finding In Normal mentioning

confidence: 99%

Maternal serum soluble CD30 is increased in pregnancies complicated with acute pyelonephritis

Kusanovic

Romero

Espinoza

et al. 2007

The Journal of Maternal-Fetal & Neonatal Medicine

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Objectives-Normal pregnancy is characterized by activation of the innate immunity and suppression of the adaptive limb of the immune response. However, pregnant women are more susceptible to the effects of infection and microbial products than non-pregnant women. CD30 is a member of the tumor necrosis factor receptor superfamily and is preferentially expressed by activated T cells producing Th2-type cytokines. Its soluble form (sCD30) is proposed to be an index of Th2 immune response. High serum concentrations of sCD30 have been found in the acute phase of viral infections, such as HIV-1 and hepatitis B. There is, however, conflicting evidence about serum sCD30 concentration in patients with bacterial infections. The objective of this study was to determine whether there are changes in the serum concentration of sCD30 in pregnant women with pyelonephritis.Methods-This cross-sectional study included normal pregnant women (N=89) and pregnant women with pyelonephritis (N=41). Maternal serum concentration of sCD30 was measured by a specific and sensitive enzyme-linked immunoassay. Non-parametric tests were used for comparisons. A p value <0.05 was considered statistically significant.Results-(1) Pregnant women with pyelonephritis had a significantly higher median serum concentration of sCD30 than those with a normal pregnancy (median: 44.3 U/ml, range: 16-352.5 vs. median: 29.7 U/ml, range: 12.2-313.2, respectively; p<0.001); and (2) No significant differences were found in the median maternal serum concentration of sCD30 between pregnant women with pyelonephritis who had a positive blood culture compared to those with a negative blood culture (median:47.7 U/mL, range: 17.1-118.8 vs. median: 42.6 U/mL, range: 16-352.5, respectively; p=0.86

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Blood Clotting Activation During Normal Pregnancy

Cited by 65 publications

References 9 publications

Plasma Fibrinogen Is a Natural Deterrent to Amyloid β-Induced Platelet Activation and Neuronal Toxicity

Plasma Fibrinogen Is a Natural Deterrent to Amyloid β-Induced Platelet Activation and Neuronal Toxicity

Normal pregnancy is characterized by systemic activation of the complement system

Maternal serum soluble CD30 is increased in pregnancies complicated with acute pyelonephritis

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