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Article ; Online: A sweet deal: blocking NMDAR for safer t-PA in diabetes.

Denorme, Frederik

2024 Volume 8, Issue 5, Page(s) 1328–1329

MeSH term(s)	Animals ; Mice ; Mice, Obese ; Hemorrhage ; Stroke ; Diabetes Mellitus ; Inflammation
Language	English
Publishing date	2024-03-12
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023012523
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Zs.A 7153: Show issues

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Article ; Online: Platelets net neutrophils during ALI.

Denorme, Frederik / Campbell, Robert A

Blood

2024 Volume 142, Issue 17, Page(s) 1409–1410

MeSH term(s)	Humans ; Neutrophil Infiltration ; Neutrophils ; Acute Lung Injury ; Blood Platelets
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2023021641
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Uh III Zs.140: 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)
Zs.MO 364: Show issues

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Article ; Online: Procoagulant platelets: novel players in thromboinflammation.

Denorme, Frederik / Campbell, Robert A

American journal of physiology. Cell physiology

2022 Volume 323, Issue 4, Page(s) C951–C958

Abstract: Platelets play a key role in maintaining hemostasis. However, dysregulated platelet activation can lead to pathological thrombosis or bleeding. Once a platelet gets activated, it will either become an aggregatory platelet or eventually a procoagulant ... ...

Abstract	Platelets play a key role in maintaining hemostasis. However, dysregulated platelet activation can lead to pathological thrombosis or bleeding. Once a platelet gets activated, it will either become an aggregatory platelet or eventually a procoagulant platelet with both types playing distinct roles in thrombosis and hemostasis. Although aggregatory platelets have been extensively studied, procoagulant platelets have only recently come into the spotlight. Procoagulant platelets are a subpopulation of highly activated platelets that express phosphatidylserine and P-selectin on their surface, allowing for coagulation factors to bind and thrombin to be generated. In recent years, novel roles for procoagulant platelets have been identified and they have increasingly been implicated in thromboinflammatory diseases. Here, we provide an up-to-date review on the mechanisms resulting in the formation of procoagulant platelets and how they contribute to hemostasis, thrombosis, and thromboinflammation.
MeSH term(s)	Blood Coagulation ; Blood Platelets/metabolism ; Humans ; Inflammation/metabolism ; P-Selectin/metabolism ; Phosphatidylserines/metabolism ; Platelet Activation ; Thrombin/metabolism ; Thromboinflammation ; Thrombosis
Chemical Substances	P-Selectin ; Phosphatidylserines ; Thrombin (EC 3.4.21.5)
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00252.2022
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Article ; Online: Immunothrombosis in neurovascular disease.

Denorme, Frederik / Ajanel, Abigail / Campbell, Robert A

Research and practice in thrombosis and haemostasis

2023 Volume 8, Issue 1, Page(s) 102298

Abstract: A State of the Art lecture titled "Immunothrombosis in Neurovascular Diseases" was presented at the International Society on Thrombosis and Haemostasis Congress in 2023. Despite significant clinical advancements in stroke therapy, stroke remains a ... ...

Abstract	A State of the Art lecture titled "Immunothrombosis in Neurovascular Diseases" was presented at the International Society on Thrombosis and Haemostasis Congress in 2023. Despite significant clinical advancements in stroke therapy, stroke remains a prominent contributor to both mortality and disability worldwide. Brain injury resulting from an ischemic stroke is a dynamic process that unfolds over time. Initially, an infarct core forms due to the abrupt and substantial blockage of blood flow. In the subsequent hours to days, the surrounding tissue undergoes gradual deterioration, primarily driven by sustained hypoperfusion, programmed cell death, and inflammation. While anti-inflammatory strategies have proven highly effective in experimental models of stroke, their successful translation to clinical use has proven challenging. To overcome this translational hurdle, a better understanding of the distinct immune response driving ischemic stroke brain injury is needed. In this review article, we give an overview of current knowledge regarding the immune response in ischemic stroke and the contribution of immunothrombosis to this process. We discuss therapeutic approaches to overcome detrimental immunothrombosis in ischemic stroke and how these can be extrapolated to other neurovascular diseases, such as Alzheimer's disease and multiple sclerosis. Finally, we summarize relevant new data on this topic presented during the 2023 International Society on Thrombosis and Haemostasis Congress.
Language	English
Publishing date	2023-12-20
Publishing country	United States
Document type	Journal Article
ISSN	2475-0379
ISSN (online)	2475-0379
DOI	10.1016/j.rpth.2023.102298
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Article ; Online: Platelet mitochondria: the mighty few.

Ajanel, Abigail / Campbell, Robert A / Denorme, Frederik

Current opinion in hematology

2023 Volume 30, Issue 5, Page(s) 167–174

Abstract: Purpose of review: Platelet mitochondrial dysfunction is both caused by, as well as a source of oxidative stress. Oxidative stress is a key hallmark of metabolic disorders such as dyslipidemia and diabetes, which are known to have higher risks for ... ...

Abstract	Purpose of review: Platelet mitochondrial dysfunction is both caused by, as well as a source of oxidative stress. Oxidative stress is a key hallmark of metabolic disorders such as dyslipidemia and diabetes, which are known to have higher risks for thrombotic complications. Recent findings: Increasing evidence supports a critical role for platelet mitochondria beyond energy production and apoptosis. Mitochondria are key regulators of reactive oxygen species and procoagulant platelets, which both contribute to pathological thrombosis. Studies targeting platelet mitochondrial pathways have reported promising results suggesting antithrombotic effects with limited impact on hemostasis in animal models. Summary: Targeting platelet mitochondria holds promise for the reduction of thrombotic complications in patients with metabolic disorders. Future studies should aim at validating these preclinical findings and translate them to the clinic.
MeSH term(s)	Animals ; Humans ; Blood Platelets/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Hemostasis ; Thrombosis/etiology ; Thrombosis/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2023-07-17
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000772
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Zs.A 3703: Show issues

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Article ; Online: Shining a light on platelet activation in COVID-19.

Denorme, Frederik / Ajanel, Abigail / Campbell, Robert A

Journal of thrombosis and haemostasis : JTH

2022 Volume 20, Issue 6, Page(s) 1286–1289

MeSH term(s)	COVID-19 ; Humans ; Platelet Activation ; SARS-CoV-2
Language	English
Publishing date	2022-03-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.15678
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 295: Show issues

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Article ; Online: Mechanisms of immunothrombosis in COVID-19.

Portier, Irina / Campbell, Robert A / Denorme, Frederik

Current opinion in hematology

2021 Volume 28, Issue 6, Page(s) 445–453

Abstract: Purpose of review: Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus-2. Over the past year, COVID-19 has posed a significant threat to global health. Although the infection is associated ...

Abstract	Purpose of review: Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus-2. Over the past year, COVID-19 has posed a significant threat to global health. Although the infection is associated with mild symptoms in many patients, a significant proportion of patients develop a prothrombotic state due to a combination of alterations in coagulation and immune cell function. The purpose of this review is to discuss the pathophysiological characteristics of COVID-19 that contribute to the immunothrombosis. Recent findings: Endotheliopathy during COVID-19 results in increased multimeric von Willebrand factor release and the potential for increased platelet adhesion to the endothelium. In addition, decreased anticoagulant proteins on the surface of endothelial cells further alters the hemostatic balance. Soluble coagulation markers are also markedly dysregulated, including plasminogen activator inhibitor-1 and tissue factor, leading to COVID-19 induced coagulopathy. Platelet hyperreactivity results in increased platelet-neutrophil and -monocyte aggregates further exacerbating the coagulopathy observed during COVID-19. Finally, the COVID-19-induced cytokine storm primes neutrophils to release neutrophil extracellular traps, which trap platelets and prothrombotic proteins contributing to pulmonary thrombotic complications. Summary: Immunothrombosis significantly contributes to the pathophysiology of COVID-19. Understanding the mechanisms behind COVID-19-induced coagulopathy will lead to future therapies for patients.
MeSH term(s)	Blood Coagulation Disorders/epidemiology ; Blood Coagulation Disorders/pathology ; Blood Coagulation Disorders/virology ; COVID-19/complications ; COVID-19/transmission ; COVID-19/virology ; Humans ; Prognosis ; SARS-CoV-2/isolation & purification ; Thrombosis/epidemiology ; Thrombosis/pathology ; Thrombosis/virology
Language	English
Publishing date	2021-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000666
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Zs.A 3703: Show issues

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Article ; Online: Targeting Glycoprotein VI for Thromboembolic Disorders.

Denorme, Frederik / Rondina, Matthew T

Arteriosclerosis, thrombosis, and vascular biology

2019 Volume 39, Issue 5, Page(s) 839–840

MeSH term(s)	Platelet Aggregation ; Platelet Membrane Glycoproteins
Chemical Substances	Platelet Membrane Glycoproteins
Language	English
Publishing date	2019-04-24
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.119.312621
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Zs.A 1705: Show issues

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Article ; Online: Brothers in arms: platelets and neutrophils in ischemic stroke.

Denorme, Frederik / Rustad, John L / Campbell, Robert A

Current opinion in hematology

2021 Volume 28, Issue 5, Page(s) 301–307

Abstract: Purpose of review: In this review, we will describe how the combined ability of platelets and neutrophils to interact with each other drives ischemic stroke brain injury.: Recent findings: Neutrophils are one of the first cells to respond during ... ...

Abstract	Purpose of review: In this review, we will describe how the combined ability of platelets and neutrophils to interact with each other drives ischemic stroke brain injury. Recent findings: Neutrophils are one of the first cells to respond during ischemic stroke. Although animals stroke models have indicated targeting neutrophils improves outcomes, clinical trials have failed to yield successful strategies. Platelets play a critical role in recruiting neutrophils to sites of injury by acting as a bridge to the injured endothelium. After initial platelet adhesion, neutrophils can rapidly bind platelets through P-selectin and glycoprotein Ibα. In addition, recent data implicated platelet phosphatidylserine as a novel key regulator of platelet-neutrophil interactions in the setting of ischemic stroke. Inhibition of procoagulant platelets decreases circulating platelet-neutrophil aggregates and thereby reduces infarct size. Platelet binding alters neutrophil function, which contributes to the injury associated with ischemic stroke. This includes inducing the release of neutrophil extracellular traps, which are neurotoxic and pro-thrombotic, leading to impaired stroke outcomes. Summary: Platelet-neutrophil interactions significantly contribute to the pathophysiology of ischemic stroke brain injury. Better understanding the mechanisms behind their formation and the downstream consequences of their interactions will lead to improved therapies for stroke patients.
MeSH term(s)	Animals ; Blood Platelets/metabolism ; Blood Platelets/pathology ; Extracellular Traps/metabolism ; Humans ; Ischemic Stroke/metabolism ; Ischemic Stroke/pathology ; Neutrophil Activation ; Neutrophils/metabolism ; Neutrophils/pathology ; P-Selectin/metabolism ; Platelet Adhesiveness ; Platelet Glycoprotein GPIb-IX Complex/metabolism
Chemical Substances	P-Selectin ; Platelet Glycoprotein GPIb-IX Complex ; SELP protein, human ; adhesion receptor
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000665
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Zs.A 3703: Show issues

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Article ; Online: Pretreatment with a dual antiplatelet and anticoagulant (APAC) reduces ischemia-reperfusion injury in a mouse model of temporary middle cerebral artery occlusion-implications for neurovascular procedures.

Denorme, Frederik / Frösen, Juhana / Jouppila, Annukka / Lindgren, Antti / Resendiz-Nieves, Julio C / Manninen, Hannu / De Meyer, Simon F / Lassila, Riitta

Acta neurochirurgica

2024 Volume 166, Issue 1, Page(s) 137

Abstract: Background: Several neurovascular procedures require temporary occlusion of cerebral arteries, leading to ischemia of unpredictable length, occasionally causing brain infarction. Experimental models of cerebral ischemia-reperfusion injury have ... ...

Abstract	Background: Several neurovascular procedures require temporary occlusion of cerebral arteries, leading to ischemia of unpredictable length, occasionally causing brain infarction. Experimental models of cerebral ischemia-reperfusion injury have established that platelet adhesion and coagulation play detrimental roles in reperfusion injury following transient cerebral ischemia. Therefore, in a model of cerebral ischemia-reperfusion injury (IRI), we investigated the therapeutic potential of a dual antiplatelet and anticoagulant (APAC) heparin proteoglycan mimetic which is able to bind to vascular injury sites. Methods: Brain ischemia was induced in mice by transient occlusion of the right middle cerebral artery for 60 min. APAC, unfractionated heparin (UFH) (both at heparin equivalent doses of 0.5 mg/kg), or vehicle was intravenously administered 10 min before or 60 min after the start of ischemia. At 24 h later, mice were scored for their neurological and motor behavior, and brain damage was quantified. Results: Both APAC and UFH administered before the onset of ischemia reduced brain injury. APAC and UFH pretreated mice had better neurological and motor functions (p < 0.05 and p < 0.01, respectively) and had significantly reduced cerebral infarct sizes (p < 0.01 and p < 0.001, respectively) at 24 h after transient occlusion compared with vehicle-treated mice. Importantly, no macroscopic bleeding complications were observed in either APAC- or UFH-treated animals. However, when APAC or UFH was administered 60 min after the start of ischemia, the therapeutic effect was lost, but without hemorrhaging either. Conclusions: Pretreatment with APAC or UFH was safe and effective in reducing brain injury in a model of cerebral ischemia induced by transient middle cerebral artery occlusion. Further studies on the use of APAC to limit ischemic injury during temporary occlusion in neurovascular procedures are indicated.
MeSH term(s)	Mice ; Animals ; Anticoagulants/pharmacology ; Anticoagulants/therapeutic use ; Infarction, Middle Cerebral Artery/drug therapy ; Brain/metabolism ; Heparin/pharmacology ; Heparin/therapeutic use ; Brain Ischemia/drug therapy ; Brain Ischemia/metabolism ; Reperfusion Injury/drug therapy ; Brain Injuries
Chemical Substances	Anticoagulants ; Heparin (9005-49-6)
Language	English
Publishing date	2024-03-15
Publishing country	Austria
Document type	Journal Article
ZDB-ID	80010-7
ISSN	0942-0940 ; 0001-6268
ISSN (online)	0942-0940
ISSN	0001-6268
DOI	10.1007/s00701-024-06017-x
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