[1] PubMed ID: | 35412486 |
Disease Name: | Colitis, Ulcerative |
Sample: | UC patient-derived colonic mucosal tissues, FHCs |
Dysfunction Pattern: | Interaction( miR-552-3p/MYD88 axis) |
Validated Method: | Western Blot//Transfection//Flow Cytometry//qRT-PCR//RIP//MTT//Luciferase Report Assay//ELISA//EdU Staining |
Description: | Our data exhibited higher levels of NORAD in UC patient-derived colonic mucosal tissues and TNF-α-stimulated FHCs.NORAD acted as a miR-552-3p sponge, and miR-552-3p silencing weakened NORAD inhibition-mediated effects on TNF-α-induced FHC apoptosis, inflammation, and oxidative stress. Myeloid differentiation primary response gene 88 (MYD88) was verified as a miR-552-3p target, and MYD88 overexpression whittled miR-552-3p mimic-mediated inhibition on TNF-α-induced FHC apoptosis, inflammation, and oxidative stress. Notably, TNF-α-induced NORAD regulated the nuclear factor-κappaB (NF-κB) signaling via the miR-552-3p/MYD88 axis. |
Causality: | Yes |
Causal Description: | Functional experiments presented that NORAD inhibition impaired TNF-α-induced FHC apoptosis, inflammation, and oxidative stress. |
Clinical-realted Application: | |
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