ArticleAmerican journal of physiology. Cell physiology2024
Cenicriviroc prevents dysregulation of astrocyte/endothelial cross talk induced by ischemia and HIV-1 via inhibiting the NLRP3 inflammasome and pyroptosis.
Article in American journal of physiology. Cell physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Chemokine Networks in Blood-Brain Barrier Regulation: Bidirectional Mechanisms, Clinical Translation, and Precision Therapeutic Prospects.Biomolecules · 2026Review
- Human umbilical cord mesenchymal stem cells alleviate hypoxic-ischemia-induced white-matter injury in neonatal rats by regulating polarization of microglia.Scientific reports · 2026Article
- Review
- Methamphetamine and HIV-1 Tat Synergistically Induce Microglial Pyroptosis Via Activation of the AIM2 Inflammasome.Inflammation · 2025Article
- Huanglian Jiedu Decoction Treats Ischemic Stroke by Regulating Pyroptosis: Insights from Multi-Omics and Drug-Target Relationship Analysis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Advances in understanding the role of interleukins in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2025Review
- The role of NLRP3 inflammasome-mediated pyroptosis in astrocytes during hyperoxia-induced brain injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Benzo[a]pyrene exacerbates allergen-induced airway inflammation through NLRP3-dependent dendritic cell activation and pathogenic T helper cell polarization.Frontiers in immunology · 2025Article
- Induced neural stem cells ameliorate blood-brain barrier injury by modulating the calcium signaling pathway of astrocyte in cerebral ischemia-reperfusion rats.Frontiers in cell and developmental biology · 2025Article
- Viral reprogramming of glial metabolism as a driver of neuroinflammation.Frontiers in immunology · 2025Review
- New Therapies and Strategies to Curb HIV Infections with a Focus on Macrophages and Reservoirs.Viruses · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Blood-brain barrier (BBB) breakdown is one of the pathophysiological characteristics of ischemic stroke, which may contribute to the progression of brain tissue damage and subsequent neurological impairment. Human immunodeficiency virus (HIV)-infected individuals are at greater risk for ischemic stroke due to diminished immune function and HIV-associated vasculopathy. Studies have shown that astrocytes are involved in maintaining BBB integrity and facilitating HIV-1 infection in the brain. The present study investigated whether targeting astrocyte-endothelial cell signaling with cenicriviroc (CVC), a dual chemokine receptor (CCR)2 and CCR5 antagonist, may protect against dysregulation of cross talk between these cells after oxygen-glucose deprivation/reoxygenation (OGD/R) combined with HIV-1 infection. Permeability assay with 10 kDa fluorescein isothiocyanate (FITC)-dextran demonstrated that CVC alleviated endothelial barrier disruption in noncontact coculture of human brain microvascular endothelial cells (HBMECs) with HIV-1-infected human astrocytes, and reversed downregulation of tight junction protein claudin-5 induced by OGD/R- and HIV-1. Moreover, CVC attenuated OGD/R- and HIV-1-triggered upregulation of the NOD-like receptor protein-3 (NLRP3) inflammasome and IL-1β secretion. Treatment with CVC also suppressed astrocyte pyroptosis by attenuating cleaved caspase-1 levels and the formation of cleaved N-terminal GSDMD (N-GSDMD). Secretome profiling revealed that CVC ameliorated secretion levels of chemokine CC chemokine ligand 17 (CCL17), adhesion molecule intercellular adhesion molecule-1 (ICAM-1), and T cell activation modulator T cell immunoglobulin and mucin domain 3 (TIM-3) by astrocytes synergistically induced by OGD/R and HIV-1. Overall, these results suggest that CVC contributes to restoring astrocyte-endothelial cross interactions in an astrocyte-dependent manner via protection against NLRP3 activation and pyroptosis.
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