miR-331 inhibits CLDN2 expression and may alleviate the vascular endothelial injury induced by sepsis

Kong, Lingchen; Wu, Peng; Li, Jianzhong

doi:10.3892/etm.2020.8854

Cited by 5 publications

(1 citation statement)

References 38 publications

(38 reference statements)

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“…Previous literature displayed that miR-331-3p participated in inflammatory responses. 30 , 31 Moreover, miR-331-3p was displayed to attenuate the viability and facilitate apoptosis of the gastric cancer cells. 32 Here, we manifested that miR-331-3p inhibition abrogated the influence of UCA1 silence on LPS-stimulated cell damage in LPS-treated FHCs, suggesting that miR-331-3p might play a crucial role in UC.…”

Section: Discussionmentioning

confidence: 99%

LncRNA UCA1 Accelerates the Progression of Ulcerative Colitis via Mediating the miR-331-3p/BRD4 Axis

Rao¹,

Shao²,

Lin³

et al. 2021

IJGM

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Background Ulcerative colitis (UC) has become one of the fastest-growing severe diseases worldwide with high morbidity. This research aimed to explore the function of lncRNA UCA1 in UC progression. Methods RT-qPCR analysis was used to examine the expression of UCA1 level in colonic mucosa tissues of UC patients. Then, fetal human cells (FHCs) were stimulated by LPS to induce inflammatory injury. CCK-8, flow cytometry and ELISA were adopted to determine the influence of UCA1 depletion on cell viability, apoptosis and pro-inflammatory factors levels in LPS-induced FHCs. The interaction between UCA1 and miR-331-3p or BRD4 was confirmed by luciferase reporter assay. The expressions of key factors involved in NF-κB pathway were assessed by Western blotting. Results LncRNA UCA1 level was elevated in colonic mucosa tissues of UC patients. LPS stimulation restrained cell viability and promoted the apoptosis and inflammatory factors levels, thus inducing FHCs inflammatory injury, while these effects were partially abolished by UCA1 knockdown. Moreover, it was found that UCA1 silence improved LPS-triggered cell injury via miR-331-3p. In addition, BRD4 was directly targeted by miR-331-3p, and BRD4 deficiency neutralized the effects of miR-331-3p repression on LPS-triggered injury in LPS-treated FHCs. Conclusion Our data determined that UCA1 knockdown attenuated UC development via targeting the miR-331-3p/BRD4/NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%