Highly-expressed circ_0129657 inhibits proliferation as well as promotes apoptosis and inflammation in HBMECs after oxygen-glucose deprivation via miR-194-5p/GMFB axis

Qian, Yun; Tang, Bo; Zhang, Hao; Yang, Hui

doi:10.1080/08916934.2023.2201405

Cited by 2 publications

(1 citation statement)

References 42 publications

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“…In an oxygen–glucose deprivation (OGD)-induced HBMECs model, circ-129657 competitively bound with miR-194-5p to regulate GMFB expression. Silencing circ-129657 upregulated GMFB, promoting endothelial cell proliferation, reducing brain infarct volume, and mitigating neurological damage in MCAO mouse models (Qian et al 2023 ). While circRNA-miRNA axes have been extensively explored in cancer and neurological diseases such as Alzheimer’s and Parkinson’s, research on their role in UE is sparse.…”

Section: Discussionmentioning

confidence: 99%

circRNA-PTPN4 mediated regulation of FOXO3 and ZO-1 expression: implications for blood–brain barrier integrity and cognitive function in uremic encephalopathy

Liu,

Qin,

Zhang

2024

Cell Biol Toxicol

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Uremic encephalopathy (UE) poses a significant challenge in neurology, leading to the need to investigate the involvement of non-coding RNA (ncRNA) in its development. This study employed ncRNA-seq and RNA-seq approaches to identify fundamental ncRNAs, specifically circRNA and miRNA, in the pathogenesis of UE using a mouse model. In vitro and in vivo experiments were conducted to explore the circRNA-PTPN4/miR-301a-3p/FOXO3 axis and its effects on blood–brain barrier (BBB) function and cognitive abilities. The research revealed that circRNA-PTPN4 binds to and inhibits miR-301a-3p, leading to an increase in FOXO3 expression. This upregulation results in alterations in the transcriptional regulation of ZO-1, affecting the permeability of human brain microvascular endothelial cells (HBMECs). The axis also influences the growth, proliferation, and migration of HBMECs. Mice with UE exhibited cognitive deficits, which were reversed by overexpression of circRNA-PTPN4, whereas silencing FOXO3 exacerbated these deficits. Furthermore, the uremic mice showed neuronal loss, inflammation, and dysfunction in the BBB, with the expression of circRNA-PTPN4 demonstrating therapeutic effects. In conclusion, circRNA-PTPN4 plays a role in promoting FOXO3 expression by sequestering miR-301a-3p, ultimately leading to the upregulation of ZO-1 expression and restoration of BBB function in mice with UE. This process contributes to the restoration of cognitive abilities. Graphical Abstract 1. The circRNA-PTPN4/miR-301a-3p/FOXO3 axis is identified as a key regulator of blood–brain barrier integrity and cognitive function in uremic encephalopathy. 2. circRNA-PTPN4 sequestration of miR-301a-3p enhances FOXO3 expression, leading to upregulation of ZO-1 and improved endothelial permeability. 3. Overexpression of circRNA-PTPN4 in uremic mice restores cognitive abilities and reduces neuronal loss and inflammatory infiltration.

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Section: Discussionmentioning

confidence: 99%