The role of blood platelets in nucleoside metabolism: regulation of megakaryocyte development and platelet production

Shaw, Timothy

doi:10.1016/0027-5107(88)90073-5

Cited by 10 publications

(5 citation statements)

References 148 publications

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“…The exact mechanisms which led to the evolutionary development of nuclear endoreduplication are still obscure. Shaw [4] speculates that megakaryocytic cells became polyploid as a result of genetic damage or metabolic imbalances involving nucleoside metabolism. As nucleotide pool imbalances may cause depletion of the number of functional mitochondrial genomes per cell, this may subsequently interfere with energy metabolism.…”

Section: Endomitotic Polyploidizationmentioning

confidence: 99%

“…Their function is determined by the megakaryocytes from which they are derived [1]. Megakaryocytes have been investigated as to their morphology, biochemistry, in vitro growth and cytokine regulation, yielding important insights into haemostasis and its behaviour in certain disorders [2][3][4][5][6][7]. Trying to settle unresolved problems may be facilitated by considering evolutionary aspects ofhaemostasis [8].…”

Section: Introductionmentioning

confidence: 99%

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Megakaryocytes: origin of bleeding and thrombotic disorders

Schneider

Gattermann

1994

Eur J Clin Investigation

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Thrombocytes of lower vertebrates are nucleated diploid cells, which differentiate directly from stem cells without an interposed megakaryocytic maturation program. With increased complexity of circulatory systems and higher blood pressures, more efficient haemostasis was required. In higher vertebrates and man, megakaryocytes developed which, by way of endomitotic polyploidization, can amplify genes relevant for haemostasis and adapt platelets to different haemostatic demands. As endomitotic polyploidization is regulated by cytokines, it is also influenced by inflammatory or malignant cell growth. The responsiveness of the megakaryocyte system to various stimuli is a possible explanation for the high incidence of thrombohaemorrhagic and thromboembolic disorders in man. For example, thrombotic complications in tumour patients are due to pathologic overstimulation of megakaryocytes. Atherosclerosis is another process which may be caused by inappropriate stimulation of the megakaryocyte system. As this complication does not manifest itself during reproductive ages, it is not going to be corrected by evolution.

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Section: Endomitotic Polyploidizationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Megakaryocytes: origin of bleeding and thrombotic disorders

Schneider

Gattermann

1994

Eur J Clin Investigation

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“…Consequently, Luccioni et al [ 19881 conclude that abnormal nucleotide synthesis may, in fact, be responsible for the particular chromosomal pattern observed in colon cancers. According to Shaw [1988], because of the increased number of genome copies per cell, polyploid, polytene, and endoreduplicated cells are much better equipped than diploids to withstand toxins and mutagens. Zucker et al [1991] also suggest that certain cells signalled into G2 for a G2 arrest will escape cell death by entering a polyploidization cycle.…”

Section: Discussionmentioning

confidence: 99%

Induction of polyploidy in human lymphocytes in vitro by excess adenine, but not by adenosine

Edwards

Anderson

Phillips

1995

Environ and Mol Mutagen

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It is known that high levels of DNA precursors can be both clastogenic and mutagenic in cultured cell lines and in vivo. The purpose of the present study was to examine at an observational level the cytogenetic effects of adenine and adenosine in primary human cell cultures. Human peripheral blood lymphocytes from four donors were cultured and treated with a range of concentrations of adenine and adenosine. Although no increase in sister chromatid exchange (SCE) frequency was observed with either compound, there was a statistically significant, dose-related increase in the proportion of polyploid cells in cultures treated with adenine, but not in those treated with adenosine. Some of the polyploid metaphases found after adenine treatment contained diplochromosomes, suggesting that endoreduplication might have been involved in polyploid formation in these cells. It is concluded that a high level of adenine can cause genetic changes in human lymphocytes by interfering with mitosis, perhaps by disturbing the balance of DNA precursor pools.

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“…Yet, this still only comprises a very small fraction of blood volume, as they are individually minuscule. This derives from the fact that platelets are not themselves "true" cells but are merely cellular fragments [ 8 ]. Thus, they lack nuclei; which makes certain modifications to their signaling or effector molecules irreversible (e.g.…”

Section: Reviewmentioning

confidence: 99%

“…To this end, platelets are produced in the bone marrow and are derived from very large cells called megakaryocytes [ 10 ]. As megakaryocytes develop, they undergo a budding process that results in the release of several thousand platelets per megakaryocyte allowing for rapid replenishment in the absence of faults in platelet regulation [ 8 , 10 ].…”

Section: Reviewmentioning

confidence: 99%

Platelet function and Isoprostane biology. Should Isoprostanes be the newest member of the Orphan-ligand family?

Ting

Khasawneh

2010

J Biomed Sci

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While there have been many reports investigating the biological activity and signaling mechanisms of isoprostanes, their role in biology, particularly in platelets, appears to still be underestimated. Moreover, whether these lipids have their own receptors is still debated, despite multiple reports that discrete receptors for isporpstanes do exist on platelets, vascular tissues, amongst others. This paper provides a review of the important literature of isoprostanes and provides reasoning that isoprostanes should be classified as orphan ligands until their receptor(s) is/are identified.

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The role of blood platelets in nucleoside metabolism: regulation of megakaryocyte development and platelet production

Cited by 10 publications

References 148 publications

Megakaryocytes: origin of bleeding and thrombotic disorders

Megakaryocytes: origin of bleeding and thrombotic disorders

Induction of polyploidy in human lymphocytes in vitro by excess adenine, but not by adenosine

Platelet function and Isoprostane biology. Should Isoprostanes be the newest member of the Orphan-ligand family?

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