Home > In process > lncRNA Glelr modulates microglia inflammatory programs in association with PU.1. > print

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024 7 _ |a 10.1016/j.nbd.2026.107366
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024 7 _ |a 0969-9961
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024 7 _ |a 1095-953X
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037 _ _ |a DZNE-2026-00385
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Pradhan, Ranjit
|0 P:(DE-2719)9001438
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245 _ _ |a lncRNA Glelr modulates microglia inflammatory programs in association with PU.1.
260 _ _ |a [Amsterdam]
|c 2026
|b Elsevier
336 7 _ |a article
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520 _ _ |a Long non-coding RNAs (lncRNAs) are emerging as key regulators of brain function, but their contribution to microglial aging and neurodegenerative disease remains largely unknown. Because only 1.5% of the human genome encodes proteins, whereas the vast majority of transcripts belong to the largely unexplored non-coding RNAome, elucidating the functions of non-coding RNAs provides an unprecedented opportunity to expand the space for therapeutic discovery. We recently identified the glia-enriched lncRNA Glelr as upregulated in the aging mouse hippocampus. Here, we investigated its function in microglia and its human homolog GLELR. We found that Glelr/GLELR is expressed in both astrocytes and microglia and increases with age. Knockdown of Glelr in primary microglia led to enhanced expression of pro-inflammatory cytokines, including TNFα, and increased phagocytic activity. RNA-sequencing revealed widespread transcriptional changes enriched for TNF and complement signaling pathways. The human homolog GLELR showed conserved functions in iPSC-derived microglia, where its loss similarly promoted inflammatory gene expression and phagocytosis. Mechanistically, Glelr interacts with the microglial transcription factor PU.1, and its depletion overlapped with PU.1-driven transcriptional programs. Consistent with these findings, GLELR expression was significantly reduced in postmortem Alzheimer's disease (AD) brains, and AD-associated genes were enriched among Glelr-regulated targets. Together, our results identify Glelr/GLELR as a conserved, aging-associated lncRNA that modulates microglial inflammatory states through interaction with PU.1. This work links glial lncRNA regulation to AD-related neuroinflammation and suggests GLELR as a potential molecular target to fine-tune microglial activity in neurodegenerative diseases.
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650 _ 7 |a 3222401L13Rik/ENSG00000272070
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650 _ 7 |a Alzheimer's disease
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650 _ 7 |a Long non-coding RNA (lncRNA)
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650 _ 7 |a Microglia
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650 _ 7 |a Neuroinflammation
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650 _ 7 |a Non-coding RNAome
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650 _ 7 |a PU.1 (SPI1)
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650 _ 7 |a RNA, Long Noncoding
|2 NLM Chemicals
650 _ 7 |a Trans-Activators
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650 _ 7 |a Proto-Oncogene Proteins
|2 NLM Chemicals
650 _ 2 |a RNA, Long Noncoding: metabolism
|2 MeSH
650 _ 2 |a RNA, Long Noncoding: genetics
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Trans-Activators: metabolism
|2 MeSH
650 _ 2 |a Trans-Activators: genetics
|2 MeSH
650 _ 2 |a Proto-Oncogene Proteins: metabolism
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650 _ 2 |a Proto-Oncogene Proteins: genetics
|2 MeSH
650 _ 2 |a Inflammation: metabolism
|2 MeSH
650 _ 2 |a Inflammation: genetics
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Cells, Cultured
|2 MeSH
650 _ 2 |a Aging: metabolism
|2 MeSH
650 _ 2 |a Astrocytes: metabolism
|2 MeSH
700 1 _ |a Sakib, M Sadman
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700 1 _ |a Kaurani, Lalit
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700 1 _ |a Krüger, Dennis M
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700 1 _ |a Pena, Tonatiuh
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700 1 _ |a Burkhardt, Susanne
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700 1 _ |a Schütz, Anna-Lena
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700 1 _ |a Kronenberg-Versteeg, Deborah
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700 1 _ |a Delalle, Ivana
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700 1 _ |a Sananbenesi, Farahnaz
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700 1 _ |a Fischer, Andre
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773 _ _ |a 10.1016/j.nbd.2026.107366
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