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Article: Perspective: Collagen induced platelet activation

Pennings, Gabrielle J / Reddel, Caroline J / Chen, Vivien M / Gnanenthiran, Sonali R / Kritharides, Leonard

2023 Volume 9, Page(s) 1104744

Abstract: Colchicine has been demonstrated to reduce cardiovascular death, myocardial infarction (MI), ischemic stroke, and ischemia-driven coronary revascularization in people with coronary artery disease (CAD). These reductions were observed even in patients ... ...

Abstract	Colchicine has been demonstrated to reduce cardiovascular death, myocardial infarction (MI), ischemic stroke, and ischemia-driven coronary revascularization in people with coronary artery disease (CAD). These reductions were observed even in patients already taking antiplatelet therapy. As well as having anti-inflammatory effects, colchicine demonstrates antiplatelet effects. We propose that colchicine's antiplatelet effects primarily target collagen-induced platelet activation
Language	English
Publishing date	2023-01-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.1104744
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Article ; Online: Colchicine as a Modulator of Platelet Function: A Systematic Review.

Reddel, Caroline J / Pennings, Gabrielle J / Chen, Vivien M / Gnanenthiran, Sonali / Kritharides, Leonard

Seminars in thrombosis and hemostasis

2022 Volume 48, Issue 5, Page(s) 552–567

Abstract: The microtubule inhibitor and anti-inflammatory agent colchicine is used to treat a range of conditions involving inflammasome activation in monocytes and neutrophils, and is now known to prevent coronary and cerebrovascular events. In vitro studies ... ...

Abstract	The microtubule inhibitor and anti-inflammatory agent colchicine is used to treat a range of conditions involving inflammasome activation in monocytes and neutrophils, and is now known to prevent coronary and cerebrovascular events. In vitro studies dating back more than 50 years showed a direct effect of colchicine on platelets, but as little contemporary attention has been paid to this area, we have critically reviewed the effects of colchicine on diverse aspects of platelet biology in vitro and in vivo. In this systematic review we searched Embase, Medline, and PubMed for articles testing platelets after incubation with colchicine and/or reporting a clinical effect of colchicine treatment on platelet function, including only papers available in English and excluding reviews and conference abstracts. We identified 98 relevant articles and grouped their findings based on the type of study and platelet function test. In vitro, colchicine inhibits traditional platelet functions, including aggregation, clotting, degranulation, and platelet-derived extracellular vesicle formation, although many of these effects were reported at apparently supraphysiological concentrations. Physiological concentrations of colchicine inhibit collagen- and calcium ionophore-induced platelet aggregation and internal signaling. There have been limited studies of in vivo effects on platelets. The colchicine-platelet interaction has the potential to contribute to colchicine-mediated reduction in cardiovascular events, but there is a pressing need for high quality clinical research in this area.
MeSH term(s)	Blood Platelets ; Colchicine/pharmacology ; Colchicine/therapeutic use ; Hemostasis ; Humans ; Platelet Aggregation ; Platelet Function Tests
Chemical Substances	Colchicine (SML2Y3J35T)
Language	English
Publishing date	2022-07-26
Publishing country	United States
Document type	Journal Article ; Systematic Review
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0042-1749660
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Article: Thrombin Generation and Cancer: Contributors and Consequences.

Reddel, Caroline J / Tan, Chuen Wen / Chen, Vivien M

Cancers

2019 Volume 11, Issue 1

Abstract: The high occurrence of cancer-associated thrombosis is associated with elevated thrombin generation. Tumour cells increase the potential for thrombin generation both directly, through the expression and release of procoagulant factors, and indirectly, ... ...

Abstract	The high occurrence of cancer-associated thrombosis is associated with elevated thrombin generation. Tumour cells increase the potential for thrombin generation both directly, through the expression and release of procoagulant factors, and indirectly, through signals that activate other cell types (including platelets, leukocytes and erythrocytes). Furthermore, cancer treatments can worsen these effects. Coagulation factors, including tissue factor, and inhibitors of coagulation are altered and extracellular vesicles (EVs), which can promote and support thrombin generation, are released by tumour and other cells. Some phosphatidylserine-expressing platelet subsets and platelet-derived EVs provide the surface required for the assembly of coagulation factors essential for thrombin generation in vivo. This review will explore the causes of increased thrombin production in cancer, and the availability and utility of tests and biomarkers. Increased thrombin production not only increases blood coagulation, but also promotes tumour growth and metastasis and as a consequence, thrombin and its contributors present opportunities for treatment of cancer-associated thrombosis and cancer itself.
Language	English
Publishing date	2019-01-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers11010100
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Article ; Online: Circulating platelet-derived extracellular vesicles are decreased after remote ischemic preconditioning in patients with coronary disease: A randomized controlled trial.

Reddel, Caroline J / Pennings, Gabrielle J / Lau, Jerrett K / Chen, Vivien M / Kritharides, Leonard

Journal of thrombosis and haemostasis : JTH

2021 Volume 19, Issue 10, Page(s) 2605–2611

Abstract: Background: Brief nonharmful ischemia, remote ischemic preconditioning (RIPC) has been proposed to confer benefit to patients with coronary artery disease via unknown mechanisms.: Objectives: We aimed to investigate the effect of RIPC on circulating ... ...

Abstract	Background: Brief nonharmful ischemia, remote ischemic preconditioning (RIPC) has been proposed to confer benefit to patients with coronary artery disease via unknown mechanisms. Objectives: We aimed to investigate the effect of RIPC on circulating levels of extracellular vesicles (EVs) and global coagulation and fibrinolytic factors in patients with coronary disease. Patients/methods: Blood samples were taken from 60 patients presenting for coronary angiography enrolled in a randomized, controlled trial before and after RIPC (3 × 5 min administration of 200 mmHg sphygmomanometer on the arm, n = 31) or sham (n = 29) treatment. Most patients (n = 48) had significant coronary artery disease and all were taking at least one antiplatelet agent. Results: Remote ischemic preconditioning significantly decreased circulating levels of EVs expressing platelet markers CD41 and CD61 detected by flow cytometry in plasma, whereas no such effect was found on EVs expressing phosphatidylserine, CD62P, CD45, CD11b, CD144, CD31 Conclusions: Remote ischemic preconditioning decreased circulating levels of platelet-derived EVs in patients with coronary disease taking conventional antiplatelet therapy. This may reflect increased EV clearance/uptake or change in production. Clinical variables may alter the effectiveness of RIPC.
MeSH term(s)	Coronary Angiography ; Coronary Artery Disease/diagnosis ; Coronary Artery Disease/therapy ; Extracellular Vesicles ; Humans ; Ischemic Preconditioning ; Tissue Plasminogen Activator
Chemical Substances	Tissue Plasminogen Activator (EC 3.4.21.68)
Language	English
Publishing date	2021-08-10
Publishing country	England
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.15441
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Article ; Online: Identification of a Distinct Platelet Phenotype in the Elderly: ADP Hypersensitivity Coexists With Platelet PAR (Protease-Activated Receptor)-1 and PAR-4-Mediated Thrombin Resistance.

Gnanenthiran, Sonali R / Pennings, Gabrielle J / Reddel, Caroline J / Campbell, Heather / Kockx, Maaike / Hamilton, Justin R / Chen, Vivien M / Kritharides, Leonard

Arteriosclerosis, thrombosis, and vascular biology

2022 Volume 42, Issue 8, Page(s) 960–972

Abstract: Background: Thrombin (via PAR [protease-activated receptor]-1 and PAR-4) and ADP (via P2Y: Methods: We characterized platelet activity in community-dwelling volunteers (n=174) in the following age groups: (1) 20 to 30 (young); (2) 40 to 55 (middle- ... ...

Abstract	Background: Thrombin (via PAR [protease-activated receptor]-1 and PAR-4) and ADP (via P2Y Methods: We characterized platelet activity in community-dwelling volunteers (n=174) in the following age groups: (1) 20 to 30 (young); (2) 40 to 55 (middle-aged); (3) ≥70 years (elderly). Platelet activity was assessed by aggregometry; flow cytometry (surface markers [P-selectin: alpha granule release, CD63: dense granule release, PAC-1: measure of conformationally active GPIIb/IIIa at the fibrinogen binding site]) measured under basal conditions and after agonist stimulation [ADP, thrombin, PAR-1 agonist or PAR-4 agonist]); receptor cleavage and quantification; fluorometry; calcium flux; ELISA. Results: The elderly had higher basal platelet activation than the young, evidenced by increased expression of P-selectin, CD63, and PAC-1, which correlated with increasing inflammation (IL [interleukin]-1β/IL-6). The elderly demonstrated higher P2Y Conclusions: Aging is associated with a distinctive platelet phenotype of increased basal activation, ADP hyperreactivity, and thrombin resistance. In situ thrombin generation associated with systemic inflammation may be novel target to prevent cardiovascular disease in the elderly.
MeSH term(s)	Adenosine Diphosphate/metabolism ; Adenosine Diphosphate/pharmacology ; Aged ; Blood Platelets/metabolism ; Calcium/metabolism ; Cardiovascular Diseases/metabolism ; Humans ; Inflammation/metabolism ; Interleukin-6/metabolism ; P-Selectin/metabolism ; Phenotype ; Platelet Activation ; Platelet Aggregation ; Receptor, PAR-1/metabolism ; Receptors, Thrombin/metabolism ; Thrombin/metabolism
Chemical Substances	Interleukin-6 ; P-Selectin ; Receptor, PAR-1 ; Receptors, Thrombin ; Adenosine Diphosphate (61D2G4IYVH) ; Thrombin (EC 3.4.21.5) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.120.316772
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Zs.A 1705: Show issues

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Article: Colchicine as a Modulator of Platelet Function: A Systematic Review

Reddel, Caroline J. / Pennings, Gabrielle J. / Chen, Vivien M. / Gnanenthiran, Sonali / Kritharides, Leonard

Seminars in Thrombosis and Hemostasis

(Editorial Compilation—Part XII)

2022 Volume 48, Issue 05, Page(s) 552–567

Series title	Editorial Compilation—Part XII
Abstract	The microtubule inhibitor and anti-inflammatory agent colchicine is used to treat a range of conditions involving inflammasome activation in monocytes and neutrophils, and is now known to prevent coronary and cerebrovascular events. In vitro studies dating back more than 50 years showed a direct effect of colchicine on platelets, but as little contemporary attention has been paid to this area, we have critically reviewed the effects of colchicine on diverse aspects of platelet biology in vitro and in vivo. In this systematic review we searched Embase, Medline, and PubMed for articles testing platelets after incubation with colchicine and/or reporting a clinical effect of colchicine treatment on platelet function, including only papers available in English and excluding reviews and conference abstracts. We identified 98 relevant articles and grouped their findings based on the type of study and platelet function test. In vitro, colchicine inhibits traditional platelet functions, including aggregation, clotting, degranulation, and platelet-derived extracellular vesicle formation, although many of these effects were reported at apparently supraphysiological concentrations. Physiological concentrations of colchicine inhibit collagen- and calcium ionophore-induced platelet aggregation and internal signaling. There have been limited studies of in vivo effects on platelets. The colchicine-platelet interaction has the potential to contribute to colchicine-mediated reduction in cardiovascular events, but there is a pressing need for high quality clinical research in this area.
Keywords	colchicine ; inflammation ; platelets
Language	English
Publishing date	2022-07-01
Publisher	Thieme Medical Publishers, Inc.
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0042-1749660
Database	Thieme publisher's database

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Zs.A 1259: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Rapid Release of Interleukin-1β from Human Platelets Is Independent of NLRP3 and Caspase.

Pennings, Gabrielle J / Reddel, Caroline J / Traini, Mathew / Lam, Magdalena / Kockx, Maaike / Chen, Vivien M / Kritharides, Leonard

Thrombosis and haemostasis

2021 Volume 122, Issue 4, Page(s) 517–528

Abstract: Objective: Platelets are critical in mediating both rapid responses to injury and the development and progression of coronary disease. Several studies have shown that, after prolonged exposure to agonists, they produce and release inflammatory ... ...

Abstract	Objective: Platelets are critical in mediating both rapid responses to injury and the development and progression of coronary disease. Several studies have shown that, after prolonged exposure to agonists, they produce and release inflammatory mediators including interleukin-1β (IL-1β), via the classical pathway (NLRP3 inflammasome and caspase-1 cleavage to release active IL-1β) as described for leukocytes. This study aimed to determine whether there is rapid release of IL-1β in response to soluble platelet agonists and whether such rapid release is NLRP3- and caspase-1-dependent. Methods and results: Using flow cytometry to detect platelet activation (and release of α and dense granule contents) and the combination of Western blotting, enzyme-linked-immunosorbent assay, and immunogold labeling transmission electron and immunofluorescence microscopy, we identified that resting human platelets contain mature IL-1β. Platelets release IL-1β within minutes in response to adenosine diphosphate (ADP), collagen, and thrombin receptor agonists, but not in response to conventional NLRP3 inflammasome agonists-lipopolysaccharide and adenosine triphosphate. The rapid release of IL-1β in response to ADP and thrombin receptor agonists was independent of caspases (including caspase-1) and NLRP3. Immature and mature IL-1β were identified as low-abundance proteins on transmission electron microscopy of human platelets, and were localized to the platelet cytosol, open canalicular system, and the periphery of α granules. Conclusion: Unlike monocytes and neutrophils, human platelets are capable of rapid agonist- and time-dependent release of IL-1β by a mechanism which is independent of caspase-1 and NLRP3.
MeSH term(s)	Adenosine Diphosphate ; Blood Platelets/metabolism ; Caspase 1/metabolism ; Caspases ; Humans ; Inflammasomes ; Interleukin-1beta/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Receptors, Thrombin
Chemical Substances	Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Receptors, Thrombin ; Adenosine Diphosphate (61D2G4IYVH) ; Caspases (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2021-06-25
Publishing country	Germany
Document type	Journal Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0041-1731288
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Zs.MO 433: Show issues

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Article ; Online: Procoagulant Effects of Low-Level Platelet Activation and Its Inhibition by Colchicine.

Reddel, Caroline J / Pennings, Gabrielle J / Curnow, Jennifer L / Chen, Vivien M / Kritharides, Leonard

Thrombosis and haemostasis

2018 Volume 118, Issue 4, Page(s) 723–733

Abstract: Platelets play an important role in diseases such as cardiovascular disease and cancer, especially through their release of extracellular vesicles (EVs) and role in thrombosis. The effects of the anti-inflammatory drug colchicine on platelets are not ... ...

Abstract	Platelets play an important role in diseases such as cardiovascular disease and cancer, especially through their release of extracellular vesicles (EVs) and role in thrombosis. The effects of the anti-inflammatory drug colchicine on platelets are not well understood. We investigated the effect of colchicine on the release of pro-coagulant EVs from platelets under low-level activation. Citrated platelet-rich plasma (PRP) from healthy donors was incubated with 2 mM colchicine or vehicle at 37°C for 30 minutes with gentle rotation. The incubation conditions caused mild platelet activation (expression of CD62P and increased surface lactadherin binding) and release of EVs expressing phosphatidylserine (PS, measured by binding of lactadherin), CD61 and CD62P, both of which were attenuated by colchicine. The incubation conditions shortened the delay to fibrin generation and this correlated with elevated levels of PS+/CD61+ EVs. Removal of EVs from plasma abrogated clot formation in the overall haemostatic potential (OHP) assay. Colchicine decreased levels of both PS+/CD61+ and CD62P+ EVs and abrogated the shortened delay to fibrin generation achieved by platelet activation. Similar results were observed after incubation of PRP with 200 µM vinblastine, suggesting a microtubular effect. An alternative method of platelet activation using platelet agonists 20 µM ADP or 10 µM epinephrine also increased CD62P+ EV levels, and this too was attenuated by prior incubation with colchicine. Our novel findings demonstrate procoagulant effects of low-level platelet activation and EV formation which are inhibited by colchicine.
MeSH term(s)	Antigens, Surface/metabolism ; Blood Coagulation/drug effects ; Blood Platelets/metabolism ; Cells, Cultured ; Coagulants/pharmacology ; Colchicine/pharmacology ; Epinephrine/administration & dosage ; Hemostasis/drug effects ; Humans ; Microtubules/metabolism ; Milk Proteins/metabolism ; P-Selectin/metabolism ; Phosphatidylserines/metabolism ; Platelet Activation/drug effects ; Platelet Aggregation ; Platelet-Rich Plasma/metabolism ; Tubulin Modulators/pharmacology ; Vinblastine/administration & dosage
Chemical Substances	Antigens, Surface ; Coagulants ; MFGE8 protein, human ; Milk Proteins ; P-Selectin ; Phosphatidylserines ; SELP protein, human ; Tubulin Modulators ; Vinblastine (5V9KLZ54CY) ; Colchicine (SML2Y3J35T) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2018-03-19
Publishing country	Germany
Document type	Journal Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0038-1636915
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Uh III Zs.192: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: Rapid Release of Interleukin-1β from Human Platelets Is Independent of NLRP3 and Caspase

Pennings, Gabrielle J. / Reddel, Caroline J. / Traini, Mathew / Lam, Magdalena / Kockx, Maaike / Chen, Vivien M. / Kritharides, Leonard

Thrombosis and Haemostasis

2021 Volume 122, Issue 04, Page(s) 517–528

Abstract	Objective: Platelets are critical in mediating both rapid responses to injury and the development and progression of coronary disease. Several studies have shown that, after prolonged exposure to agonists, they produce and release inflammatory mediators including interleukin-1β (IL-1β), via the classical pathway (NLRP3 inflammasome and caspase-1 cleavage to release active IL-1β) as described for leukocytes. This study aimed to determine whether there is rapid release of IL-1β in response to soluble platelet agonists and whether such rapid release is NLRP3- and caspase-1-dependent. Methods and Results: Using flow cytometry to detect platelet activation (and release of α and dense granule contents) and the combination of Western blotting, enzyme-linked-immunosorbent assay, and immunogold labeling transmission electron and immunofluorescence microscopy, we identified that resting human platelets contain mature IL-1β. Platelets release IL-1β within minutes in response to adenosine diphosphate (ADP), collagen, and thrombin receptor agonists, but not in response to conventional NLRP3 inflammasome agonists—lipopolysaccharide and adenosine triphosphate. The rapid release of IL-1β in response to ADP and thrombin receptor agonists was independent of caspases (including caspase-1) and NLRP3. Immature and mature IL-1β were identified as low-abundance proteins on transmission electron microscopy of human platelets, and were localized to the platelet cytosol, open canalicular system, and the periphery of α granules. Conclusion: Unlike monocytes and neutrophils, human platelets are capable of rapid agonist- and time-dependent release of IL-1β by a mechanism which is independent of caspase-1 and NLRP3.
Keywords	platelet ; inflammation ; interleukin-1β ; NLRP3 ; inflammasome
Language	English
Publishing date	2021-06-25
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0041-1731288
Database	Thieme publisher's database

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Article ; Online: Elastin in asthma.

Reddel, Caroline J / Weiss, Anthony S / Burgess, Janette K

Pulmonary pharmacology & therapeutics

2012 Volume 25, Issue 2, Page(s) 144–153

Abstract: Extracellular matrix is generally increased in asthma, causing thickening of the airways which may either increase or decrease airway responsiveness, depending on the mechanical requirements of the deposited matrix. However, in vitro studies have shown ... ...

Abstract	Extracellular matrix is generally increased in asthma, causing thickening of the airways which may either increase or decrease airway responsiveness, depending on the mechanical requirements of the deposited matrix. However, in vitro studies have shown that the altered extracellular matrix produced by asthmatic airway smooth muscle cells is able to induce increased proliferation of non-asthmatic smooth muscle cells, which is a process believed to contribute to airway hyper-responsiveness in asthma. Elastin is an extracellular matrix protein that is altered in asthmatic airways, but there has been no systematic investigation of the functional effect of these changes. This review reveals divergent reports of the state of elastin in the airway wall in asthma. In some layers of the airway it has been described as increased, decreased and/or fragmented, or unchanged. There is also considerable evidence for an imbalance of matrix metalloproteinases, which degrade elastin, and their respective inhibitors the tissue inhibitors of metalloproteinases, which collectively help to explain observations of both increased elastin and elastin fragments. A loss of lung elastic recoil in asthma suggests a mechanical role for disordered elastin in the aetiology of the disease, but extensive studies of elastin in other tissues show that elastin fragments elicit cellular effects such as increased proliferation and inflammation. This review summarises the current understanding of the role of elastin in the asthmatic airway.
MeSH term(s)	Animals ; Asthma/physiopathology ; Bronchial Hyperreactivity/physiopathology ; Cell Proliferation ; Elastin/metabolism ; Extracellular Matrix/metabolism ; Humans ; Inflammation/physiopathology ; Matrix Metalloproteinases/metabolism ; Myocytes, Smooth Muscle/metabolism
Chemical Substances	Elastin (9007-58-3) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2012-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1399707-5
ISSN	1522-9629 ; 1094-5539
ISSN (online)	1522-9629
ISSN	1094-5539
DOI	10.1016/j.pupt.2012.02.001
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