Cellular Microparticles in Subarachnoid Hemorrhage

Boettinger, S; Lackner, Peter

doi:10.1007/s12975-015-0413-y

Cited by 4 publications

(5 citation statements)

References 28 publications

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“…Endothelial MV was significantly increased in SAH patients, and the increased endothelial cell MV is related with symptomatic cerebral vasospasm 143 , and predicts infarction post-SAH 150 . MVs may play an important role for secondary complications in patients with ischemic and hemorrhagic stroke 151 .…”

Section: Future Perspectivesmentioning

confidence: 99%

Brain–Heart Interaction

Chen

Venkat

Seyfried

et al. 2017

Circulation Research

420

202

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Neurocardiology is an emerging specialty that addresses the interaction between the brain and the heart, i.e. the effects of cardiac injury on the brain, and the effects of brain injury on the heart. This review article focuses on cardiac dysfunction in the setting of stroke such as ischemic stroke, brain hemorrhage and subarachnoid hemorrhage (SAH). The majority of post stroke deaths are attributed to neurological damage, and cardiovascular complications are the second leading cause of post stroke mortality. Accumulating clinical and experimental evidence suggests a causal relationship between brain damage and heart dysfunction. Thus, it is important to determine whether cardiac dysfunction is triggered by stroke, is an unrelated complication, or is the underlying cause of stroke. Stroke induced cardiac damage may lead to fatality or potentially lifelong cardiac problems (such as heart failure), or to mild and recoverable damage such as neurogenic stress cardiomyopathy (NSC) and Takotsubo cardiomyopathy. The role of location and lateralization of brain lesions after stroke in brain-heart interaction, clinical biomarkers and manifestations of cardiac complications, and underlying mechanisms of brain-heart interaction following stroke, such as: the hypothalamic pituitary adrenal axis (HPA); catecholamine surge; sympathetic and parasympathetic regulation; microvesicles (MV’s); microRNAs; gut microbiome, immunoresponse and systemic inflammation are discussed.

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Section: Future Perspectivesmentioning

confidence: 99%

Brain–Heart Interaction

Chen

Venkat

Seyfried

et al. 2017

Circulation Research

420

202

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mentioning

confidence: 99%

“…Another potential therapeutic target is cellular microparticles, which are small vesicles formed by plasma membranes of various vascular cells such as endothelial cells, smooth muscle cells, platelets, leukocytes, and erythrocytes [45]. Cellular microparticles are released from the membranes by triggers causing cellular activation or apoptosis including cytokines, hypoxia and shear stress, and transfer receptors and cytosolic contents such as enzymes, ribonucleic, and deoxyribonucleic acids to cells of different origin [45,46]. In clinical SAH, plasma levels of various cell-derived microparticles, especially tissue factor-expressing and endothelial cellassociated microparticles, were elevated at day 0 post-SAH, and the development of cerebral infarction by day 14, suggesting the linkage among inflammation, endothelial dysfunction, and thrombosis, were predicted [47].…”

mentioning

confidence: 99%

Inflammation: a Good Research Target to Improve Outcomes of Poor-Grade Subarachnoid Hemorrhage

Suzuki

2019

Transl. Stroke Res.

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“…In the context of SAH, a promising research field has recently emerged related the extracellular vesicles (EVs) [13]. Initially described as pro-coagulant "dust" surrounding activated platelets [14], EVs have been shown to be important mediators of physiological and pathological processes in various diseases.…”

Section: Introductionmentioning

confidence: 99%

Circulating Extracellular Vesicles in Subarachnoid Hemorrhage Patients: Characterization and Cellular Effects

Grossini,

Esposito,

Viretto

et al. 2023

IJMS

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Circulating extracellular vesicles (EVs) may play a pathophysiological role in the onset of complications of subarachnoid hemorrhage (SAH), potentially contributing to the development of vasospasm (VP). In this study, we aimed to characterize circulating EVs in SAH patients and examine their effects on endothelial and smooth muscle cells (SMCs). In a total of 18 SAH patients, 10 with VP (VP), 8 without VP (NVP), and 5 healthy controls (HC), clinical variables were recorded at different time points. EVs isolated from plasma samples were characterized and used to stimulate human vascular endothelial cells (HUVECs) and SMCs. We found that EVs from SAH patients expressed markers of T-lymphocytes and platelets and had a larger size and a higher concentration compared to those from HC. Moreover, EVs from VP patients reduced cell viability and mitochondrial membrane potential in HUVECs and increased oxidants and nitric oxide (NO) release. Furthermore, EVs from SAH patients increased intracellular calcium levels in SMCs. Altogether, our findings reveal an altered pattern of circulating EVs in SAH patients, suggesting their pathogenic role in promoting endothelial damage and enhancing smooth muscle reactivity. These results have significant implications for the use of EVs as potential diagnostic/prognostic markers and therapeutic tools in SAH management.

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Cellular Microparticles in Subarachnoid Hemorrhage

Cited by 4 publications

References 28 publications

Brain–Heart Interaction

Brain–Heart Interaction

Inflammation: a Good Research Target to Improve Outcomes of Poor-Grade Subarachnoid Hemorrhage

Circulating Extracellular Vesicles in Subarachnoid Hemorrhage Patients: Characterization and Cellular Effects

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