PMID- 35609334 OWN - NLM STAT- MEDLINE DCOM- 20220526 LR - 20220716 IS - 2165-5987 (Electronic) IS - 2165-5979 (Print) IS - 2165-5979 (Linking) VI - 13 IP - 5 DP - 2022 May TI - Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88. PG - 12863-12875 LID - 10.1080/21655979.2022.2077572 [doi] AB - Circular RNA (circRNA) had been confirmed to participate in ulcerative colitis (UC) development. Circular RNA_0001187 (Circ_0001187) had been found to be overexpressed in patients with Crohn disease. Therefore, circ_0001187 might be an important circRNA regulating intestinal inflammatory diseases. However, the role and mechanism of circ_0001187 in UC progression remains unclear. The colonic mucosal tissues were obtained from 23 UC patients and 23 healthy normal controls. Tumor necrosis factor-alpha (TNF-alpha) was used to mimic UC cell model in vitro. Cell function was assessed by cell counting kit 8 assay, EdU assay, flow cytometry, ELISA assay and oxidative stress detection. RNA interaction was confirmed by dual-luciferase reporter assay and RIP assay. Serum exosomes were isolated by ultracentrifugation and identified by transmission electron microscope. Circ_0001187 was overexpressed in UC patients. Circ_0001187 knockdown enhanced the proliferation, while suppressed apoptosis, inflammation and oxidative stress of TNF-alpha-induced FHC cells. Circ_0001187 acted as miR-1236-3p sponge, and the effects of circ_0001187 downregulation on TNF-alpha-induced FHC cell injury were overturned by miR-1236-3p inhibitor. MYD88 was targeted by miR-1236-3p, and circ_0001187 sponged miR-1236-3p to regulate MYD88. MYD88 knockdown alleviated TNF-alpha-induced FHC cell injury, and its upregulation revoked the inhibition effect of miR-1236-3p on TNF-alpha-induced FHC cell injury. High expression of circ_0001187 also was observed in the serum exosomes of UC patients. Our data confirmed that circ_0001187 facilitated UC progression through miR-1236-3p/MYD88 axis, which might be a potential treatment and diagnosis biomarker for UC. FAU - Ouyang, Wei AU - Ouyang W AD - Department of Oncology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou City, China. FAU - Wu, Min AU - Wu M AD - Department of Emergency, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou City, China. FAU - Wu, Anshan AU - Wu A AD - Department of Oncology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou City, China. FAU - Xiao, Heng AU - Xiao H AD - Department of Anorectal, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou City, China. LA - eng PT - Journal Article PL - United States TA - Bioengineered JT - Bioengineered JID - 101581063 RN - 0 (MIRN1236 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Myeloid Differentiation Factor 88) RN - 0 (RNA, Circular) RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - *Colitis, Ulcerative/genetics MH - Humans MH - *MicroRNAs/genetics/metabolism MH - Myeloid Differentiation Factor 88/genetics/metabolism MH - RNA, Circular/genetics MH - Tumor Necrosis Factor-alpha/genetics/metabolism PMC - PMC9275921 OTO - NOTNLM OT - MYD88 OT - Ulcerative colitis OT - circ_0001187 OT - miR-1236-3p COIS- No potential conflict of interest was reported by the author(s). EDAT- 2022/05/25 06:00 MHDA- 2022/05/27 06:00 PMCR- 2022/05/24 CRDT- 2022/05/24 17:42 PHST- 2022/05/24 17:42 [entrez] PHST- 2022/05/25 06:00 [pubmed] PHST- 2022/05/27 06:00 [medline] PHST- 2022/05/24 00:00 [pmc-release] AID - 2077572 [pii] AID - 10.1080/21655979.2022.2077572 [doi] PST - ppublish SO - Bioengineered. 2022 May;13(5):12863-12875. doi: 10.1080/21655979.2022.2077572.