bims-evecad 2025-09-14 papers

Issue of 2025–09–14
three papers selected by
Cliff Dominy

Brain Res Bull. 2025 Sep 05. pii: S0361-9230(25)00349-1. [Epub ahead of print] 111537

Microglia-Astroglia-Neuron network following stroke: novel insight into extracellular vesicles communication.

Hao Wan, Yicheng Cui, Yanyang Zeng, Jianbin Hu, Meihua Li, Zhipeng Xiao.

Stroke is one of the leading causes of death and disability worldwide, with ischemic stroke accounting for the majority of cases. Intercellular communication is critical to its prognostic impact, and extracellular vesicles (EVs) are an emerging important mechanism. EVs are increasingly recognized as key mediators of crosstalk between neurons and glial cells, affecting processes such as neuroinflammation, oxidative stress and tissue repair. More previous studies have focused on signaling and information exchange between the two types of cells. This paper reviews the EVs-mediated triad interaction between neurons, astrocytes and microglia after stroke based on the spatiotemporal entanglement of them. Not only the intercellular crosstalk of EVs of microglial, astrocytic, or neuronal origins is explored in detail, the cargoes carried by EVs and their mechanisms of action are resolved, but also the overlapping parts in the EVs-mediated cellular communication mechanisms are analyzed, such as the NF-κB signaling pathway and miR-124 which play an important and complex role in a variety of intercellular communications. On this basis, EVs were revealed to have potential as biomarkers and therapeutic carriers. The aim of this paper is to contribute to our deeper understanding of stroke pathophysiology and to inspire new possible therapeutic strategies.

Keywords: Stroke; astrocyte; extracellular vesicles; microglia; neuron

DOI: https://doi.org/10.1016/j.brainresbull.2025.111537

J Atheroscler Thromb. 2025 Sep 09.

Blood Cells, Endothelial Cells, and Circulating Extracellular Vesicles Induce Procoagulant Activity by Phosphatidylserine Exposure in Chronic Coronary Artery Disease Patients with In-stent Restenosis after Percutaneous Coronary Intervention.

Dongxia Tong, Lu Kong, Bin Song, Wei Wu, Guangwen Li, Fangyu Xie, Haiyang Wang, Chunquan Zhang, Yvhao Liu, Yibing Shao, Wei Xia, Jihe Li.

AIMS: In-stent restenosis (ISR) is a significant limitation of coronary stent implantation, but the exact mechanism of ISR remains unclear. Patients after percutaneous coronary intervention (PCI) are in a hypercoagulable state; however, there is less information on its association with chronic coronary artery disease (CAD) in patients with ISR after PCI. We aimed to clarify whether or not CAD patients with ISR after PCI are in a hypercoagulable state and whether or not PS exposure on extracellular vesicles (EVs), blood cells (BCs), and endothelial cells (ECs) is involved in the hypercoagulable state.
METHODS: Phosphatidylserine (PS) exposure to EVs, BCs, and ECs was analyzed using flow cytometry. Procoagulant activity (PCA) was analyzed by clotting time (CT), purified clotting complex assays, and fibrin production assays.
RESULTS: Compared with pre-PCI or controls, levels of exposed PS on EVs, BCs, and ECs were significantly increased from 1 day, peaked at 3 months, and gradually decreased within 1 year in CAD patients after PCI, especially in CAD patients with ISR after PCI. Furthermore, their increased levels significantly decrease CT and enhance intrinsic/extrinsic FXa, thrombin, and fibrin generation. PCA was weakened by approximately 80% when lactadherin was used.
CONCLUSIONS: Our results revealed that CAD patients after PCI, especially those patients with ISR after PCI, are associated with a hypercoagulable state in which PS exposure on EVs, BCs, and ECs plays a more important role than tissue factors. Therefore, blocking PS exposure to EVs, BCs, and ECs may provide a new target for preventing ISR in these patients.

Keywords: Chronic coronary artery disease; Extracellular vesicles; In-stent restenosis; Percutaneous coronary intervention; Procoagulant activity

DOI: https://doi.org/10.5551/jat.65577

Cell Physiol Biochem. 2025 Sep 06. 59(5): 589-608

Migrasomes in Health and Disease: Insights into Mechanisms, Pathogenesis, and Therapeutic Opportunities.

Lauryn Akeme, Pollyanna Sibanda, Aisling Fitzgerald, Agnieszka Bossowska, Klaudia Bonowicz, Dominika Jerka, Maciej Gagat.

Migrasomes are newly discovered, migration-dependent organelles that mediate the release of cellular contents into the extracellular environment through a process known as migracytosis. Since their identification in 2014, growing evidence has highlighted their critical roles in intercellular communication, organ development, mitochondrial quality control, and disease pathogenesis. Migrasome biogenesis is a complex, multi-step process tightly regulated by lipid composition, tetraspanin-enriched microdomains, and molecular pathways involving sphingomyelin synthase 2, Rab35, and integrins. Unlike exosomes, migrasomes possess distinct structural and functional characteristics, which position them as novel organelles rather than classic extracellular vesicles. Recent studies have revealed their involvement in diverse pathological contexts, including kidney disease, cancer progression, proliferative vitreoretinopathy, viral infections, and myocardial infarction. Notably, migrasomes hold promise as diagnostic biomarkers, especially in early podocyte injury, and as therapeutic targets in oncology and regenerative medicine. This review summarizes the current understanding of migrasome biology, and their implications in health and disease, and explores emerging perspectives on harnessing migrasomes for diagnostic and therapeutic applications.

Keywords: Migrasomes ; Migracytosis ; Intercellular communication ; Tetraspanins

DOI: https://doi.org/10.33594/000000810