Long noncoding RNA Gpr137b-ps mediates 15-PGDH-induced angiogenesis in brain microvasculature following tMCAO in mice.
D, W., G, Z., H, G., Y, W., W, L., Y, C., & Y, J. (2026). Long noncoding RNA Gpr137b-ps mediates 15-PGDH-induced angiogenesis in brain microvasculature following tMCAO in mice.. PloS one. https://doi.org/10.1371/journal.pone.0349591
D W, G Z, H G, Y W, W L, Y C, et al. Long noncoding RNA Gpr137b-ps mediates 15-PGDH-induced angiogenesis in brain microvasculature following tMCAO in mice.. PloS one. 2026; doi: 10.1371/journal.pone.0349591
D W, G Z, H G, et al. Long noncoding RNA Gpr137b-ps mediates 15-PGDH-induced angiogenesis in brain microvasculature following tMCAO in mice.[J]. PloS one. 2026. DOI: 10.1371/journal.pone.0349591.
@article{d2026,
author = {Wang D and Zhang G and Gou H and Wang Y and Liang W and Cao Y and Jiao Y},
title = {Long noncoding RNA Gpr137b-ps mediates 15-PGDH-induced angiogenesis in brain microvasculature following tMCAO in mice.},
journal = {PloS one},
year = {2026},
doi = {10.1371/journal.pone.0349591},
note = {PMID: 42497132},
}
TY - JOUR AU - Wang D AU - Zhang G AU - Gou H AU - Wang Y AU - Liang W AU - Cao Y AU - Jiao Y TI - Long noncoding RNA Gpr137b-ps mediates 15-PGDH-induced angiogenesis in brain microvasculature following tMCAO in mice. T2 - PloS one PY - 2026 DO - 10.1371/journal.pone.0349591 AN - PMID:42497132 ER -
BACKGROUND: Angiogenesis is essential for recovery following ischemic stroke, as brain microvascular endothelial cells (BMVECs) drive vascular repair. 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is a major regulator of endothelial function in some vascular contexts, but it is unknown whether 15-PGDH plays a significant role in angiogenesis following stroke. Notably, based on preliminary bioinformatics prediction of their 3'UTR interaction, we hypothesize that Gpr137b-ps-a pseudogene-derived lncRNA originating from Gpr137b-forms a regulatory link with 15-PGDH to modulate this process (i.e., post-stroke angiogenesis) by regulating 15-PGDH expression, though its specific functional mechanism in this context remains largely unknown. METHODS: To address this gap, we used mouse middle cerebral artery occlusion (MCAO) model in vivo and BMVEC oxygen-glucose deprivation/reoxygenation (OGD/R) model in vitro. We modulated 15-PGDH via siRNA and Gpr137b-ps via mimics, and assessed angiogenesis using migration, tube formation, and cell-cycle assays, with expression and localization of key molecules verified by standard molecular techniques. RESULTS: Both MCAO and OGD/R successfully induced ischemia, with significant upregulation of 15-PGDH and Gpr137b-ps in ischemic tissues and BMVECs (P < 0.05). Despite this concurrent upregulation, 15-PGDH promoted angiogenesis (silencing reduced BMVEC proliferation, migration, and tube formation; P < 0.01), whereas Gpr137b-ps overexpression suppressed 15-PGDH protein levels and inhibited angiogenesis-effects that were rescued by re-expressing 15-PGDH. CONCLUSION: Together, our findings identify Gpr137b-ps/15-PGDH as a key feedback regulatory axis: while both Gpr137b-ps and 15-PGDH are upregulated under ischemia, Gpr137b-ps (a negative regulator of angiogenesis) suppresses 15-PGDH (a pro-angiogenic factor) to repress excessive post-stroke angiogenesis via inhibiting BMVEC proliferation, migration, and cell-cycle progression. The data support an association and partial dependency between this axis and angiogenic processes, highlighting it as a potential therapeutic target (e.g., via inhibiting Gpr137b-ps) for vascular repair after ischemic stroke.