Overwhelming evidence suggests that platelets have a detrimental role in promoting cancer spread via platelet-cancer cell interactions linked to thrombotic mechanisms. On the other hand, a beneficial role of platelets in the preservation of the endothelial barrier in inflammatory conditions has been recently described, a phenomenon that could also operate in cancer-related inflammation. It is tempting to speculate that some antiplatelet strategies to combat cancer metastasis may impair the endogenous platelet-dependent mechanisms preserving endothelial barrier function. If the protective function of platelets is impaired, it may lead to increased endothelial permeability and more efficient cancer cell intravasation in the primary tumor and cancer cell extravasation at metastatic sites. In this commentary, we discuss current evidence that could support this hypothesis.
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http://dx.doi.org/10.1016/j.bcp.2020.113886 | DOI Listing |
Alzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: The Neurovascular Unit is a multicellular structure of the CNS known to become dysfunctional in Alzheimer's Disease (AD) and cerebral amyloid angiopathy. Amyloidosis disrupts the function of cerebrovascular endothelial cells (cECs) via extrinsic and intrinsic apoptosis, and induction of blood brain barrier (BBB) permeability. Findings in our lab demonstrated that pan-Carbonic Anhydrase inhibitors (CAi's) prevent mitochondria-mediated apoptotic mechanisms in cECs.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Institute of Chinese Medical Sciences, State Key Laboratory of Quality Research in Chinese Medicine, University of Macau, Taipa, Macau SAR, China.
Bone marrow mesenchymal stem cells (BMSCs) -derived extracellular vesicles (EVs), especially small EVs (sEVs), were vastly reported to enable multiple restorative effects on ischemic stroke, yet the protective mechanism of blood-brain barrier (BBB) has not been fully illustrated. In the present study, we investigated the therapeutic effects and mechanism of BMSCs-derived sEVs on BBB injury after ischemic stroke. In-vivo, administering sEVs to transient middle cerebral artery occlusion (tMCAo) mice mitigated the brain infarct volume, BBB permeability and neural apoptosis, and improved the cerebral blood flow perfusion and neurological function.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, 92697, USA.
Background: Immunothrombosis is the process by which the coagulation cascade interacts with the innate immune system to control infection. However, the formation of clots within the brain vasculature can be detrimental to the host. Recent work has demonstrated that Toxoplasma gondii infects and lyses central nervous system (CNS) endothelial cells that form the blood-brain barrier (BBB).
View Article and Find Full Text PDFAdv Med Sci
January 2025
Department of Histology and Embryology, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, Toruń, Poland; Faculty of Medicine, Collegium Medicum, Mazovian Academy in Płock, Płock, Poland.
Purpose: Proper functioning of the endothelial barrier is crucial for cardiovascular system homeostasis. Oxidative stress can lead to endothelial dysfunction (ED), damaging lipids, proteins, and DNA. Reactive oxygen species also increase cytoplasmic Ca levels, activating transient receptor potential melastatin 2 (TRPM2), a membrane non-selective calcium channel.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Introduction: We investigated the specific factors driving abnormal angiogenesis in Alzheimer's disease (AD) and its role in cerebrovascular lesions and neurodegeneration.
Methods: We assessed cerebrovascular pathologies, amyloid-beta (Aβ), and tau pathologies in post mortem human brains and detected 12 angiogenic factors in cerebrospinal fluid (CSF) from the China Aging and Neurodegenerative Disease Initiative (CANDI) cohort.
Results: We observed severe blood-brain barrier damage and elevated levels of the vascular marker CD31 in human AD brains, which had a stronger correlation with tau pathology than Aβ pathology.
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