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长链非编码 RNA BZRAP1-AS1 通过调节 miR-1286/COL5A2 轴缓解类风湿关节炎。

lncRNA BZRAP1-AS1 alleviates rheumatoid arthritis by regulating miR-1286/COL5A2 axis.

机构信息

Department of Pain Medicine, Wuhan University of Science and Technology Affiliated Puren Hospital, Wuhan, Hubei, China.

Department of Traditional Chinese Medicine, Wuhan Pulmonary Hospital, Wuhan, Hubei, China.

出版信息

Immun Inflamm Dis. 2022 Feb;10(2):163-174. doi: 10.1002/iid3.558. Epub 2021 Nov 11.

DOI:10.1002/iid3.558
PMID:34766472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8767512/
Abstract

BACKGROUND

Dysregulation of BZRAP1-AS1 was associated with immune statuses of cancer or Alzheimer's disease patients, yet little is known about its role in rheumatoid arthritis.

METHODS

RT-qPCR and western blot were applied to assess the expression of indicated expression. CCK-8 and BrdU proliferation assays were used to measure the proliferation of RA-HFLS. Apoptosis in RA-HFLS was evidenced by the alteration of caspase-3 activity and apoptosis-related factors. ELISA was performed to detect IL-6, IL-1β, and TNF-α level. Luciferase reporter, RIP, and pull-down assays were used to confirm the BZRAP1-AS1/miR-1286/COL5A2 cascade predicted by bioinformatics analysis.

RESULTS

BZRAP1-AS1 and COL5A2 were downregulated in RA tissues and RA-HFLS while miR-1286 was amplified. Overexpression of BZRAP1-AS1 reduced the RA-HFLS proliferation, IL-6, IL-1β, and TNF-α level and induced cell apoptosis while BZRAP1-AS1 silence produced an opposite effect. Overexpression of BZRAP1-AS1 reduced the miR-1286 expression which in turn increased the COL5A2 expression, thereby relieving the excessive proliferation and limited apoptosis in RA-HFLS.

CONCLUSION

Our findings suggested that BZRAP1-AS1 sequestered miR-1286 and reshaped the COL5A2 expression, thereby suppressed RA-HFLS proliferation and inflammation, and triggered cell apoptosis, resulting in the attenuation of RA progression.

摘要

背景

BZRAP1-AS1 的失调与癌症或阿尔茨海默病患者的免疫状态有关，但关于其在类风湿关节炎中的作用知之甚少。

方法

应用 RT-qPCR 和 Western blot 评估指示表达的表达。CCK-8 和 BrdU 增殖测定用于测量 RA-HFLS 的增殖。通过 caspase-3 活性和凋亡相关因子的改变来证明 RA-HFLS 中的凋亡。通过 ELISA 检测 IL-6、IL-1β 和 TNF-α 水平。使用荧光素酶报告、RIP 和下拉测定来证实生物信息学分析预测的 BZRAP1-AS1/miR-1286/COL5A2 级联。

结果

BZRAP1-AS1 和 COL5A2 在 RA 组织和 RA-HFLS 中下调，而 miR-1286 扩增。BZRAP1-AS1 的过表达减少了 RA-HFLS 的增殖、IL-6、IL-1β 和 TNF-α 水平并诱导细胞凋亡，而 BZRAP1-AS1 沉默则产生相反的效果。BZRAP1-AS1 的过表达降低了 miR-1286 的表达，从而增加了 COL5A2 的表达，从而减轻了 RA-HFLS 中的过度增殖和有限凋亡。

结论

我们的研究结果表明，BZRAP1-AS1 隔离了 miR-1286 并重塑了 COL5A2 的表达，从而抑制了 RA-HFLS 的增殖和炎症，并触发了细胞凋亡，从而减轻了 RA 的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/f52d82530929/IID3-10-163-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/63656530ad47/IID3-10-163-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/9a9453d44ae1/IID3-10-163-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/7dd9085400bc/IID3-10-163-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/9866d7455600/IID3-10-163-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/f61813771416/IID3-10-163-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/f52d82530929/IID3-10-163-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/63656530ad47/IID3-10-163-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/9a9453d44ae1/IID3-10-163-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/7dd9085400bc/IID3-10-163-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/9866d7455600/IID3-10-163-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82a/8767512/f61813771416/IID3-10-163-g005.jpg
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