bioRxivNeurosciencePreprint
Japanese Encephalitis Virus Infected Microglial Cells Secrete Exosomes Containing let-7a/b that Facilitate Neuronal Damage via Caspase Activation
Sriparna MukherjeeiD, Irshad AkbariD, Bharti KumariiD, Sudhanshu VratiiD, Anirban BasuiD, Arup Kumar BanerjeeiD
Abstract
Extracellular microRNAs (miRNAs) are essential for the cell to cell communication in the healthy and diseased brain. MicroRNAs released from the activated microglia upon neurotropic virus infection may exacerbate CNS damage. Here, we identified let-7a and let-7b (let-7a/b) as the overexpressed miRNAs in Japanese Encephalitis virus (JEV) infected microglia and assessed their role in JEV pathogenesis. We measured the let-7a/b expressions in JEV infected post-mortem human brains, mice brains and in mouse microglial N9 cells by the qRT-PCR and in situ hybridization assay. The interaction between let-7a/b and NOTCH signaling pathway further examined in Toll-like receptor 7 knockdown (TLR7 KD) mice to assess the functions. Exosomes released from JEV infected or let-7a/b mimic transfected N9, and HEK-293 cells were isolated and evaluated their function. We observed an upregulation of let-7a/b in the infected brains as well as in microglia. Knockdown of TLR7 or Inhibition of let-7a/b suppressed the JEV induced NOTCH activation possibly via NF-{kappa}B dependent manner and subsequently, attenuated JEV induced TNF production in microglial cells. Further, exosomes secreted from JEV-infected microglial cells specifically contained let-7a/b. Exosomes overexpressed with let-7a/b were injected into BALB/c mice as well as co-incubated with mouse neuronal (Neuro2a) cells, or primary cortical neuron resulted in caspase activation leading to neuronal damage in the brain. Thus, our results provide evidence for the multifaceted role of let-7a/b miRNAs and unravel the exosomes mediated mechanism for JEV induced pathogenesis.
- Citations
- 1
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Degradation of miR-466d-3p by JEV NS3 facilitates viral replication and IL-1β expression
- Endophilin mediated endocytosis and Epidermal growth factor receptor govern Japanese encephalitis virus entry and infection in neuronal cells
Puja Sharma, Mukesh Tanwar, … Manjula Kalia·PLoS PathogensPeer-reviewed·Dec 16, 2025
- Lipid Droplets mediated Japanese Encephalitis Virus small Extracellular Vesicle Release
Bhaghyasree Mallick, Ankita Sarkar, … Sourish Ghosh·bioRxiv·Nov 4, 2025
- Methotrimeprazine exerts antiviral and neuroprotective effects in Japanese encephalitis virus infection through activation of adaptive ER stress and autophagy
S. K. Prajapat, L. Mishra, … M. Kalia·bioRxiv·Apr 5, 2023
- Alpha-synuclein expression in neuron modulates the Japanese encephalitis virus infection
A. Gupta, A. Mohapatra, … S. Kumar·bioRxiv·Sep 25, 2023
- Spatial transcriptomics elucidates the central role of cerebral vasculatures in the progression of Japanese encephalitis
Zhihua Ou, Zhaoyang Wang, … Gong Cheng·bioRxiv·Mar 6, 2025