ArticleEmerging microbes & infections2018
miR-1303 regulates BBB permeability and promotes CNS lesions following CA16 infections by directly targeting MMP9.
Article in Emerging microbes & infections, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Circulating Brain-Related miRNAs as Predictors of Postoperative Delirium in Cardiac Surgery Patients.International journal of molecular sciences · 2025Article
- The key mechanisms of multi-system responses triggered by central nervous system damage in hand, foot, and mouth disease severity.Infectious medicine · 2024Review
- Analysis of miRNAs involved in mouse brain injury upon Coxsackievirus A6 infection.Frontiers in cellular and infection microbiology · 2024Article
- IP-10 acts early in CV-A16 infection to induce BBB destruction and promote virus entry into the CNS by increasing TNF-α expression.Frontiers in immunology · 2024Article
- The Correlation Between Peripheral Blood Micro-Ribonucleic Acid Expression Level and Personality Disorder in Patients with Schizophrenia.Alpha psychiatry · 2024Article
- Astrocyte Involvement in Blood-Brain Barrier Function: A Critical Update Highlighting Novel, Complex, Neurovascular Interactions.International journal of molecular sciences · 2023Review
- Insight on Bacterial Newborn Meningitis Using a Neurovascular-Unit-on-a-Chip.Microbiology spectrum · 2023Article
- The Effects of Viruses on Insulin Sensitivity and Blood-Brain Barrier Function.International journal of molecular sciences · 2023Review
- MicroRNA expression profile of human umbilical vein endothelial cells in response to coxsackievirus A10 infection reveals a potential role of miR-143-3p in maintaining the integrity of the blood-brain barrier.Frontiers in cellular and infection microbiology · 2023Article
- Article
- Comprehensive profiling and characterization of cellular microRNAs in response to coxsackievirus A10 infection in bronchial epithelial cells.Virology journal · 2022Article
- Roles of Non-Coding RNAs in Virus-Host Interaction About Pathogenesis of Hand-Foot-Mouth Disease.Current microbiology · 2022Review
- Mechanisms of hypoxia in the hippocampal CA3 region in postoperative cognitive dysfunction after cardiopulmonary bypass.Journal of cardiothoracic surgery · 2022Article
- Non-coding RNAs in the regulation of blood-brain barrier functions in central nervous system disorders.Fluids and barriers of the CNS · 2022Review
- The role of immune cells and associated immunological factors in the immune response to spinal cord injury.Frontiers in immunology · 2022Review
- Involvement of host microRNAs in flavivirus-induced neuropathology: An update.Journal of biosciences · 2022Review
- miRNA nanoencapsulation to regulate the programming of the blood-brain barrier permeability by hypoxia.Current research in pharmacology and drug discovery · 2022Review
- Zika Virus NS1 Suppresses VE-Cadherin and Claudin-5 via hsa-miR-101-3p in Human Brain Microvascular Endothelial Cells.Molecular neurobiology · 2021Article
- Non-coding RNAs: the extensive and interactive regulators of the blood-brain barrier permeability.RNA biology · 2021Review
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Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
Coxsackievirus A16 (CA16) is a member of the Picornaviridae family and causes mild and self-limiting hand, foot, and mouth disease (HFMD) in infants and young children. CA16 infection can also progress to central nervous system (CNS) complications; however, the underlying mechanism by which CA16 penetrates the blood-brain barrier (BBB) and then causes CNS damage remains unclear. This study aimed to explore the mechanism of CA16 neurotropic tropism by establishing an in vitro BBB model with CA16 infection and an in vivo CA16 rhesus monkey infant infection model. The results showed that CA16 infection induced increased permeability of the BBB accompanied by upregulation of matrix metalloproteinase 9 (MMP9) expression. Subsequently, high-throughput miRNA sequencing technology and bioinformatics analysis revealed that miR-1303 may regulate BBB permeability by targeting MMP9. Next, we used dual-luciferase, qRT-PCR, and western blot assays to provide evidence of MMP9 targeting by miR-1303. Further experiments revealed that CA16 infection promoted the degradation of junctional complexes (Claudin4, Claudin5, VE-Cadherin, and ZO-1), likely by downregulating miR-1303 and upregulating MMP9. Finally, EGFP-CA16 infection could enter the CNS by facilitating the degradation of junctional complexes, eventually causing neuroinflammation and injury to the CNS, which was confirmed using the in vivo rhesus monkey model. Our results indicate that CA16 might penetrate the BBB and then enter the CNS by downregulating miR-1303, which disrupts junctional complexes by directly regulating MMP9 and ultimately causing pathological CNS changes. These results provide new therapeutic targets in HFMD patients following CA16 infection.
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