Elemental composition of platelets. Part II. Water content of normal human platelets and measurements of their concentrations of Cu, Fe, K, and Zn by neutron activation analysis.

Kiem, J.; Borberg, H.; Iyengar, G. V.; Kasperek, K.; Siegers, M.; Feinendegen, L. E.; Gross, R.

doi:10.1093/clinchem/25.5.705

Cited by 31 publications

(4 citation statements)

References 14 publications

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“…Therefore, about half of the Zn 2+ in platelets is released when platelets are activated. This represents ~ 5 µM Zn 2+ released by the equivalent number of platelets normally in blood, consistent with previous reports (24,25). Therefore, when platelets are activated and aggregate at the site of injury, the local concentration of Zn 2+ can increase above the 10-20 µM reported in platelet-poor plasma (6)(7)(8).…”

Section: Quantification Of Zn 2+ In Platelets and Platelet Releasatesupporting

confidence: 90%

Zinc delays clot lysis by attenuating plasminogen activation and plasmin-mediated fibrin degradation

Henderson¹,

Stafford²,

Leslie³

et al. 2015

Thromb Haemost

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Zinc circulates free in plasma at a concentration of 0.1-2 µM, but its levels increase locally when it is released from activated platelets. Although zinc influences many processes in haemostasis, its effect on fibrinolysis has not been thoroughly investigated. Using a fluorescent zinc-binding probe, we demonstrated that zinc binds tissue-type plasminogen activator (tPA) and plasmin with high affinity (Kd values of 0.2 µM), and surface plasmon resonance studies revealed that zinc binds fibrin with a Kd of 12.8 µM. Zinc had no effect on the affinity of plasminogen or plasmin for fibrin, but increased the affinity of tPA by two-fold. In the presence of 5 µM zinc, the catalytic efficiency of plasminogen activation by tPA was reduced by approximately two-fold, both in the absence or presence of fibrin. Zinc attenuated plasmin-mediated degradation of the fibrinogen alpha-chain by 43 %, but had no effect on trypsin degradation. tPA-mediated fibrin clot lysis was prolonged 2.5-fold by zinc in a concentration-dependent fashion, and tPA-mediated plasma clot lysis was attenuated by 1.5-fold. Therefore, our data indicate that zinc modulates fibrinolysis by attenuating tPA-mediated plasminogen activation and plasmin-induced fibrin degradation. These findings suggest that local release of zinc by platelets attenuates fibrinolysis.

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Section: Quantification Of Zn 2+ In Platelets and Platelet Releasatesupporting

confidence: 90%

Zinc delays clot lysis by attenuating plasminogen activation and plasmin-mediated fibrin degradation

Henderson¹,

Stafford²,

Leslie³

et al. 2015

Thromb Haemost

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“…They found iron deficiency anemia in women caused arachidonic acid induced platelet dysfunction through iron-containing enzymes may give rise to increased menstrual blood loss, which can be reversed through iron repletion. Kiem et al 12 showed that iron is present in platelets in a concentration of approximately 12.28 µg/g, further supporting the hypothesis of Karpatkin and colleagues 13 that iron may have a functional role in controlling platelet production.…”

Section: Discussionmentioning

confidence: 64%

Triad of Iron Deficiency Anemia, Severe Thrombocytopenia and Menorrhagia–-A Case Report and Literature Review

Ibrahim

Khan

Raza

et al. 2012

Clin Med Insights Case Rep

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Introduction Thrombocytosis is a common disorder in patients diagnosed with iron deficiency anemia. The decreased platelet counts commonly found iron deficiency anemia is rarely reported in clinical practice. The exact mechanism of the occurrence of thrombocytopenia in iron deficiency anemia remains unclear. In this case report we discuss a triad of symptoms seen in the African American population: Iron deficiency anemia, menorrhagia and thrombocytopenia. Case presentation A 40 year old multiparous African-American woman presented with heavy vaginal bleed, severe anemia (3.5 g/dL) and thrombocytopenia (30,000/mm3). The peripheral blood smear showed marked microcytic hypochromic cells with decreased platelets counts. After excluding other causes of thrombocytopenia and anemia, increased red cell distribution width and low iron saturation confirmed the diagnosis of iron deficiency anemia. Treatment for iron deficiency anemia was initiated with intravenous and oral iron supplements. Two months following treatment of iron deficiency anemia, the triad of manifestations resolved and patient remained stable. Conclusion Profound degree of iron deficiency anemia can present with thrombocytopenia and severe menorrhagia. Iron replacement should be the main treatment goal in these patients. This case report further supports the 2 compartment model of the role of iron in maintaining platelet counts.

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“…In further support of this conclusion, it has been shown that APC inactivates factor Va much more efficiently on artificial phospholipid membranes or endothelial cells than on platelets (38). Cu 2+ ions, which are also found in platelets, may contribute to such effect (39).…”

Section: Discussionmentioning

confidence: 78%

Zinc ions bind to and inhibit activated protein C

et al. 2010

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SummaryZn 2+ ions were found to efficiently inhibit activated protein C (APC), suggesting a potential regulatory function for such inhibition. APC activity assays employing a chromogenic peptide substrate demonstrated that the inhibition was reversible and the apparent K I was 13 ± 2 µM. k cat was seven fold decreased whereas K M was unaffected in the presence of 10 µM Zn 2+. The inhibitory effect of Zn 2+ on APC activity was also observed when factor Va was used as a substrate in an assay coupled to a prothrombinase assay. The interaction of Zn 2+ with APC was accompanied by a reversible ∼40% decrease in tryptophan fluorescence, consistent with the ion inducing a conformational change in the protein. The apparent K D was 7.4 ± 1.5 µM and thus correlated well with the apparent K I . In the presence of physiological Ca 2+ concentration the K I and K D values were three to four fold enhanced, presum- . Comparisons of sequences and structures suggested several possible sites for zinc binding. The magnitude of the apparent K I in relation to the blood and platelet concentrations of Zn 2+ supports a physiological role for this ion in the regulation of anticoagulant activity of APC. These findings broaden the understanding of this versatile serine protease and enable the future development of potentially more efficient anticoagulant APC variants for treatments of thrombotic diseases.

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Elemental composition of platelets. Part II. Water content of normal human platelets and measurements of their concentrations of Cu, Fe, K, and Zn by neutron activation analysis.

Cited by 31 publications

References 14 publications

Zinc delays clot lysis by attenuating plasminogen activation and plasmin-mediated fibrin degradation

Zinc delays clot lysis by attenuating plasminogen activation and plasmin-mediated fibrin degradation

Triad of Iron Deficiency Anemia, Severe Thrombocytopenia and Menorrhagia–-A Case Report and Literature Review

Zinc ions bind to and inhibit activated protein C

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