Pericytes are mural cells of blood microvessels which play a crucial role at the neurovascular interface of the central nervous system. They are involved in the regulation of blood-brain barrier integrity, angiogenesis, clearance of toxic metabolites, capillary hemodynamic responses, and neuroinflammation, and they demonstrate stem cell activity. Morphological and molecular studies to characterize brain pericytes recently pointed out some heterogeneity in pericyte population. Nevertheless, a clear definition of pericyte subtypes is still lacking. Here, we demonstrate that a fraction of brain pericytes express Connexin 30 (Cx30), a gap junction protein, which, in the brain parenchyma, was thought to be exclusively found in astrocytes. Cx30 could thus be a candidate protein in the composition of the gap junction channels already described between endothelial cells and pericytes. It could also form hemichannels or acts in a channel-independent manner to regulate pericyte morphology, as already observed in astrocytes. Altogether, our results suggest that Cx30 defines a novel brain pericyte subtype.
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http://dx.doi.org/10.1007/s00429-017-1562-4 | DOI Listing |
Alzheimers Dement
January 2025
UK Dementia Research Institute at the University of Edinburgh, Edinburgh, UK.
Introduction: Cerebrovascular dysfunction plays a critical role in the pathogenesis of dementia and related neurodegenerative disorders. Recent omics-driven research has revealed associations between vascular abnormalities and transcriptomic alterations in brain vascular cells, particularly endothelial cells (ECs) and pericytes (PCs). However, the impact of these molecular changes on dementia remains unclear.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Research Group on Tumors of the Central Nervous System, Pathology Department, University of Valencia, 46010 Valencia, Spain.
Glioblastoma IDH wild type (GB), the most common malignant primary brain tumor, is characterized by rapid proliferation, extensive infiltration into surrounding brain tissue, and significant resistance to current therapies. Median survival is only 15 months despite extensive clinical efforts. The tumor microenvironment (TME) in GB is highly specialized, supporting the tumor's aggressive behavior and its ability to evade conventional treatments.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Biochemistry, Molecular Biology B and Immunology Department, University of Murcia (UMU), 30120 Murcia, Spain.
Glioblastoma (GB) is one of the most aggressive and treatment-resistant cancers due to its complex tumor microenvironment (TME). We previously showed that GB progression is dependent on the aberrant induction of chaperone-mediated autophagy (CMA) in pericytes (PCs), which promotes TME immunosuppression through the PC secretome. The secretion of extracellular matrix (ECM) proteins with anti-tumor (Lumican) and pro-tumoral (Osteopontin, OPN) properties was shown to be dependent on the regulation of GB-induced CMA in PCs.
View Article and Find Full Text PDFEur Cytokine Netw
September 2024
The blood-brain barrier (BBB) consists of a unique system of brain microvascular endothelial cells, capillary basement membranes, and terminal branches ("end-feet") of astrocytes. The BBB's primary function is to protect the central nervous system from potentially harmful or toxic substances in the bloodstream by selectively controlling the entry of cells and molecules, including nutrients and immune system components. During neuroinflammation, the BBB loses its integrity, resulting in increased permeability, mostly due to the activity of inflammatory cytokines.
View Article and Find Full Text PDFStroke
December 2024
Department of Neurology, Institut de Psychiatrie et Neurosciences de Paris, INSERM U1266, GHU Paris Psychiatrie et Neurosciences, Université Paris Cité, France.
Reperfusion injury (RI) refers to an array of detrimental cellular and biochemical processes that are widely believed to be triggered by reperfusion following focal cerebral ischemia and to contribute to infarct extension and poor outcome despite complete recanalization. Accordingly, it is widely recommended that therapies targeting RI be administered after recanalization. The present topical review demonstrates, however, that the vast majority of, and possibly all, processes considered part of RI are not actually provoked by reperfusion but develop during the ischemic phase.
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