Effects of Primary Mast Cell Disease on Hemostasis and Erythropoiesis

Seidel, H.; Hertfelder, Hans‐Jörg; Oldenburg, Johannes; Kruppenbacher, J. P.; Afrin, Lawrence B.; Molderings, Gerhard J.

doi:10.3390/ijms22168960

Cited by 14 publications

(9 citation statements)

References 71 publications

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“…The increase of mast cells may also affect the relatively high occurrence of pulmonary embolisms in COVID‐19, as mast cells were found to induce thrombosis through activation of clotting factors and platelets. 30 , 31 Taken together, these results suggest that tryptase‐ and chymase‐positive mast cells may play a role in pulmonary fibrosis and embolisms in COVID‐19.…”

Section: Discussionmentioning

confidence: 84%

“…Interestingly, tryptase‐ and chymase‐positive mast cells are also increased in CLAD and other diseases with involvement of pulmonary fibrosis, 27–29 suggesting that both diseases have similar underlying biological processes. The increase of mast cells may also affect the relatively high occurrence of pulmonary embolisms in COVID‐19, as mast cells were found to induce thrombosis through activation of clotting factors and platelets 30,31 . Taken together, these results suggest that tryptase‐ and chymase‐positive mast cells may play a role in pulmonary fibrosis and embolisms in COVID‐19.…”

Section: Discussionmentioning

confidence: 89%

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Increase of mast cells in COVID‐19 pneumonia may contribute to pulmonary fibrosis and thrombosis

et al. 2022

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Aims Lung tissue from COVID‐19 patients shares similar histomorphological features with chronic lung allograft disease, also suggesting activation of autoimmune‐related pathways in COVID‐19. To more clearly understand the underlying spectrum of pathophysiology in COVID‐19 pneumonia, we analysed mRNA expression of autoimmune‐related genes in post‐mortem lung tissue from COVID‐19 patients. Methods and results Formalin‐fixed, paraffin‐embedded lung tissue samples of 18 COVID‐19 patients and eight influenza patients were used for targeted gene expression profiling using NanoString technology. Multiplex immunofluorescence for tryptase and chymase was applied for validation. Genes related to mast cells were significantly increased in COVID‐19. This finding was strengthened by multiplex immunofluorescence also showing a significant increase of tryptase‐ and chymase‐positive cells in COVID‐19. Furthermore, receptors for advanced glycation end‐products (RAGE) and pro‐platelet basic protein (PPBP) were up‐regulated in COVID‐19 compared to influenza. Genes associated with Type I interferon signalling showed a significant correlation to detected SARS‐CoV2 pathway‐related genes. The comparison of lung tissue samples from both groups based on the presence of histomorphological features indicative of acute respiratory distress syndrome did not result in finding any specific gene or pathways. Conclusion Two separate means of measuring show a significant increase of mast cells in SARS‐CoV‐2‐infected lung tissue compared to influenza. Additionally, several genes involved in fibrosis and thrombosis, among which are RAGE and PPBP, are up‐regulated in COVID‐19. As mast cells are able to induce thrombosis and fibrosis, they may play an important role in the pathogenesis of COVID‐19.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 89%

Increase of mast cells in COVID‐19 pneumonia may contribute to pulmonary fibrosis and thrombosis

et al. 2022

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“…Thrombotic aggregates of mast cells have been found to surround blood vessels and provide many important repair molecules, including heparin, tissue plasminogen activator (a fibrinolytic precursor), and beta-trypsin (a fibrinolytic protease). Thus, recruitment and activation of mast cells may lead to local thrombolysis and the prevention of clotting ( 78 ). When drug-induced mast cell inactivation or depletion leads to the inhibition of the vascular repair system, thromboembolism and arterial stenosis events become more likely to occur ( 79 ).…”

Section: Preclinical Studiesmentioning

confidence: 99%

Coronary atherosclerosis and chemotherapy: From bench to bedside

Zhou

Zhu

Liu

et al. 2023

Front. Cardiovasc. Med.

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Cardiovascular disease, particularly coronary artery disease, is the leading cause of death in humans worldwide. Coronary heart disease caused by chemotherapy affects the prognosis and survival of patients with tumors. The most effective chemotherapeutic drugs for cancer include proteasome inhibitors, tyrosine kinase inhibitors, immune checkpoint inhibitors, 5-fluorouracil, and anthracyclines. Animal models and clinical trials have consistently shown that chemotherapy is closely associated with coronary events and can cause serious adverse cardiovascular events. Adverse cardiovascular events after chemotherapy can affect the clinical outcome, treatment, and prognosis of patients with tumors. In recent years, with the development of new chemotherapeutic drugs, new discoveries have been made about the effects of drugs used for chemotherapy on cardiovascular disease and its related mechanisms, such as inflammation. This review article summarizes the effects of chemotherapeutic drugs on coronary artery disease and its related mechanisms to guide efforts in reducing cardiovascular adverse events during tumor chemotherapy, preventing the development of coronary heart disease, and designing new prevention and treatment strategies for cardiotoxicity caused by clinical tumor chemotherapy.

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“…The O- and N-sulfation of these disaccharide units lead to the high negative charge of these GAGs ( Scheme 1 ) [ 1 ]. Heparins are commonly found in the granules of mast cells, and heparan sulfates are ubiquitously present in the extracellular matrix of a wide variety of animal tissues and organs [ 2 , 3 ]. These polyanionic GAGs interact with a diverse array of biomolecular and biological targets, including extracellular matrix and cell surface components, growth factors, proteases, protease inhibitors, and various pathogens [ 4 , 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Metal Binding to Sodium Heparin Monitored by Quadrupolar NMR

Sieme¹,

Griesinger²,

Rezaei‐Ghaleh

2022

IJMS

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Heparins and heparan sulfate polysaccharides are negatively charged glycosaminoglycans and play important roles in cell-to-matrix and cell-to-cell signaling processes. Metal ion binding to heparins alters the conformation of heparins and influences their function. Various experimental techniques have been used to investigate metal ion-heparin interactions, frequently with inconsistent results. Exploiting the quadrupolar 23Na nucleus, we herein develop a 23Na NMR-based competition assay and monitor the binding of divalent Ca2+ and Mg2+ and trivalent Al3+ metal ions to sodium heparin and the consequent release of sodium ions from heparin. The 23Na spin relaxation rates and translational diffusion coefficients are utilized to quantify the metal ion-induced release of sodium ions from heparin. In the case of the Al3+ ion, the complementary approach of 27Al quadrupolar NMR is employed as a direct probe of ion binding to heparin. Our NMR results demonstrate at least two metal ion-binding sites with different affinities on heparin, potentially undergoing dynamic exchange. For the site with lower metal ion binding affinity, the order of Ca2+ > Mg2+ > Al3+ is obtained, in which even the weakly binding Al3+ ion is capable of displacing sodium ions from heparin. Overall, the multinuclear quadrupolar NMR approach employed here can monitor and quantify metal ion binding to heparin and capture different modes of metal ion-heparin binding.

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Effects of Primary Mast Cell Disease on Hemostasis and Erythropoiesis

Cited by 14 publications

References 71 publications

Increase of mast cells in COVID‐19 pneumonia may contribute to pulmonary fibrosis and thrombosis

Increase of mast cells in COVID‐19 pneumonia may contribute to pulmonary fibrosis and thrombosis

Coronary atherosclerosis and chemotherapy: From bench to bedside

Metal Binding to Sodium Heparin Monitored by Quadrupolar NMR

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