{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T06:40:39Z","timestamp":1792737639033,"version":"4.5.0"},"reference-count":42,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2019,1,31]],"date-time":"2019-01-31T00:00:00Z","timestamp":1548892800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100010803","name":"Department of Biotechnology, Government of West Bengal","doi-asserted-by":"publisher","award":["BT\/PR22341\/MED\/122\/55\/2016"],"award-info":[{"award-number":["BT\/PR22341\/MED\/122\/55\/2016"]}],"id":[{"id":"10.13039\/501100010803","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010803","name":"Department of Biotechnology, Government of West Bengal","doi-asserted-by":"publisher","award":["BT\/PR6714\/MED\/29\/617\/2012"],"award-info":[{"award-number":["BT\/PR6714\/MED\/29\/617\/2012"]}],"id":[{"id":"10.13039\/501100010803","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010803","name":"Department of Biotechnology, Government of West Bengal","doi-asserted-by":"publisher","award":["BT\/HRD\/35\/01\/02\/2014"],"award-info":[{"award-number":["BT\/HRD\/35\/01\/02\/2014"]}],"id":[{"id":"10.13039\/501100010803","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2019,5]]},"abstract":"Abstract<\/jats:title>\n \n \n \n Micro\n RNA<\/jats:styled-content>\n s (mi\n RNA<\/jats:styled-content>\n s) released from the activated microglia upon neurotropic virus infection may exacerbate the neuronal damage. Here, we identified\n let\u20107a<\/jats:italic>\n and\n let\u20107b<\/jats:italic>\n (\n let\u20107a\/b<\/jats:italic>\n ) as one of the essential mi\n RNA<\/jats:styled-content>\n s over\u2010expressed upon Japanese Encephalitis virus (\n JEV<\/jats:styled-content>\n ) infection and released in the culture supernatant of the\n JEV<\/jats:styled-content>\n \u2010infected microglial cells through extracellular vesicles. The\n let\u20107a\/b<\/jats:italic>\n was previously reported to modulate inflammation in microglial cells through Toll\u2010like receptor 7 (\n TLR<\/jats:styled-content>\n 7) pathways; although their role in accelerating\n JEV<\/jats:styled-content>\n pathogenesis remain unexplored. Therefore, we studied the role of\n let\u20107a\/b<\/jats:italic>\n in modulating microglia\u2010mediated inflammation during\n JEV<\/jats:styled-content>\n infection and investigated the effect of\n let\u20107a\/b<\/jats:italic>\n \u2010containing exosomes on primary neurons. To this end, we examined\n let\u20107a\/b<\/jats:italic>\n and\n NOTCH<\/jats:styled-content>\n signaling pathway in\n TLR<\/jats:styled-content>\n 7 knockdown (\n KD<\/jats:styled-content>\n ) mice. We observed that\n TLR<\/jats:styled-content>\n 7\n KD<\/jats:styled-content>\n or inhibition of\n let\u20107a\/b<\/jats:italic>\n suppressed the\n JEV<\/jats:styled-content>\n \u2010induced\n NOTCH<\/jats:styled-content>\n activation possibly via\n NF<\/jats:styled-content>\n \u2010\u03baB dependent manner and subsequently, attenuated\n JEV<\/jats:styled-content>\n \u2010induced\n TNF<\/jats:styled-content>\n \u03b1 production in microglial cells. Furthermore, exosomes secreted from\n let\u20107a\/b<\/jats:italic>\n over\u2010expressed microglia when transferred to uninfected mice brain induced caspase activation. Exosomes secreted from virus\u2010infected or\n let\u20107a\/b<\/jats:italic>\n over\u2010expressed microglia when co\u2010incubated with mouse neuronal (Neuro2a) cells or primary cortical neurons also facilitated caspase activation leading to neuronal death. Thus, our results provide evidence for the multifaceted role of\n let\u20107a\/b<\/jats:italic>\n mi\n RNA<\/jats:styled-content>\n s in\n JEV<\/jats:styled-content>\n pathogenesis.\n Let\u20107a\/b<\/jats:italic>\n can interact with\n TLR<\/jats:styled-content>\n 7 and\n NOTCH<\/jats:styled-content>\n signaling pathway and enhance\n TNF<\/jats:styled-content>\n \u03b1 release from microglia. On the other hand, the exosomes secreted by\n JEV<\/jats:styled-content>\n \u2010infected microglia can activate caspases in uninfected neuronal cells which possibly contribute to bystander neuronal death.\n <\/jats:p>\n <\/jats:sec>\n \n \n \n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n \n Cover Image for this issue: doi:\n 10.1111\/jnc.14506<\/jats:ext-link>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/jnc.14645","type":"journal-article","created":{"date-parts":[[2018,12,17]],"date-time":"2018-12-17T10:26:07Z","timestamp":1545042367000},"page":"518-534","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":78,"title":["Japanese Encephalitis Virus\u2010induced\n let\u20107a\/b<\/i>\n interacted with the\n NOTCH<\/scp>\n \u2010\n TLR<\/scp>\n 7 pathway in microglia and facilitated neuronal death via caspase activation"],"prefix":"10.1111","volume":"149","author":[{"given":"Sriparna","family":"Mukherjee","sequence":"first","affiliation":[{"name":"National Brain Research Center Manesar India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irshad","family":"Akbar","sequence":"additional","affiliation":[{"name":"National Brain Research Center Manesar India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bharti","family":"Kumari","sequence":"additional","affiliation":[{"name":"Translational Health Science and Technology Institute Faridabad India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sudhanshu","family":"Vrati","sequence":"additional","affiliation":[{"name":"Translational Health Science and Technology Institute Faridabad India"},{"name":"Regional Center for Biotechnology Faridabad 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