LncRNA-ZNF252P-AS1/miR-15b-5p promotes the proliferation of keloid fibroblast by regulating the BTF3-STAT3 signaling pathway

Yu, Xiao‐Qi; Li, Mengjuan; Long, Junling; Fan, Pengcheng; Zuo, Chenchen; Wang, Yongjie

doi:10.1016/j.jdermsci.2022.12.010

Cited by 2 publications

(3 citation statements)

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“…However, it enhanced the binding of STAT3 to BTF3 and the phosphorylation of STAT3, demonstrating that the binding efficiency positively modulated the pathway. One the other side, BTF3 has been reported to regulate the level of p‐STAT3/STAT3 but does not change the total STAT3 43,52 . Consistently, our findings showed that BTF3 interference downregulated p‐STAT3/STAT3 levels.…”

Section: Discussionsupporting

confidence: 89%

“…One the other side, BTF3 has been reported to regulate the level of p-STAT3/STAT3 but does not change the total STAT3. 43,52 Consistently, our findings showed that BTF3 interference downregulated p-STAT3/STAT3 levels.…”

Section: Discussionsupporting

confidence: 86%

“…However, the relationship between HSPA1B, TUBA1C, YTHDF3, SRP68, AP1B1, HYOU1 and pyroptosis has not been reported. BTF3, a basic transcription factor, has been shown to promote STAT3 phosphorylation, and activated STAT3 signalling potentially modulates NLRP3‐mediated pyroptosis and associated inflammation 43,44 . Thus, the transcription factors BTF3 and STAT3 were of particular interest.…”

Section: Resultsmentioning

confidence: 99%

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ARID5B‐mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti‐β2GPI‐treated monocytes

Tan,

Qiao,

Yang

et al. 2024

Clinical & Translational Med

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BackgroundAlterations of the trimethylation of histone 3 lysine 4 (H3K4me3) mark in monocytes are implicated in the development of autoimmune diseases. Therefore, the purpose of our study was to elucidate the role of H3K4me3‐mediated epigenetics in the pathogenesis of antiphospholipid syndrome (APS).MethodsH3K4me3 Cleavage Under Targets and Tagmentation and Assay for Transposase‐Accessible Chromatin were performed to determine the epigenetic profiles. Luciferase reporter assay, RNA immunoprecipitation, RNA pull‐down, co‐immunoprecipitation and chromatin immunoprecipitation were performed for mechanistic studies. Transmission electron microscopy and propidium iodide staining confirmed cell pyroptosis. Primary monocytes from patients with primary APS (PAPS) and healthy donors were utilised to test the levels of key molecules. A mouse model mimicked APS was constructed with beta2‐glycoprotein I (β2GPI) injection. Blood velocity was detected using murine Doppler ultrasound.ResultsH3K4me3 signal and open chromatin at the ARID5B promoter were increased in an in vitro model of APS. The epigenetic factor ARID5B directly activated LINC01128 transcription at its promoter. LINC01128 promoted the formation of the BTF3/STAT3 complex to enhance STAT3 phosphorylation. Activated STAT3 interacted with the NLRP3 promoter and subsequently stimulated pyroptosis and apoptosis. ARID5B or BTF3 depletion compensated for LINC01128‐induced pyroptosis and apoptosis by inhibiting STAT3 phosphorylation. In mice with APS, β2GPI exposure elevated the levels of key proteins of pyroptosis and apoptosis pathways in bone marrow‐derived monocytes, reduced the blood velocity of the ascending aorta, increased the thrombus size of the carotid artery, and promoted the release of interleukin (IL)‐18, IL‐1β and tissue factor. Patients with PAPS had the high‐expressed ARID5B and LINC01128, especially those with triple positivity for antiphospholipid antibodies. Moreover, there was a positive correlation between ARID5B and LINC01128 expression.ConclusionThis study indicated that ARID5B/LINC01128 was synergistically upregulated in APS, and they aggravated disease pathogenesis by enhancing the formation of the BTF3/STAT3 complex and boosting p‐STAT3‐mediated pyroptosis and apoptosis, thereby providing candidate therapeutic targets for APS.Highlights The H3K4me3 mark and chromatin accessibility at the ARID5B promoter are increased in vitro model mimicked APS. ARID5B‐mediated LINC01128 induces pyroptosis and apoptosis via p‐STAT3 by binding to BTF3. ARID5B is high‐ expressed in patients with primary APS and positively correlated with LINC01128 expression. OICR‐9429 treatment mitigates pyroptosis and related inflammation in vivo and in vitro models mimicked APS.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 86%

Section: Resultsmentioning

confidence: 99%

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