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长链非编码 RNA MALAT1 通过 miR-135b-5p/GPNMB 轴调控帕金森病细胞模型中的细胞增殖和凋亡。

Long non-coding RNA MALAT1 regulates cell proliferation and apoptosis via miR-135b-5p/GPNMB axis in Parkinson's disease cell model.

机构信息

Department of Neurology, Affiliated Dongguan People's Hospital, Southern Medical University (Dongguan People's Hospital), Guangdong Province, 523059, Dongguan, People's Republic of China.

Department of General Practice, Affiliated Dongguan People's Hospital, Southern Medical University (Dongguan People's Hospital), 3 South Wandao Road, Wanjiang District, 523059, Dongguan, Guangdong Province, People's Republic of China.

出版信息

Biol Res. 2021 Mar 16;54(1):10. doi: 10.1186/s40659-021-00332-8.

DOI:10.1186/s40659-021-00332-8
PMID:33726823
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7968316/
Abstract

BACKGROUNDS

Parkinson's disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD.

METHODS

SK-N-SH and SK-N-BE cells were treated with MPP to establish the MPP-stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP-stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP-stimulated cell model of PD were explored.

RESULTS

MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis.

CONCLUSION

Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP-stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.

摘要

背景

帕金森病（PD）是一种常见的与年龄相关的神经退行性疾病，在全球范围内都有发生。本研究旨在探讨长链非编码 RNA 转移相关肺腺癌转录本 1（MALAT1）在 PD 中的作用及其机制。

方法

用 MPP 处理 SK-N-SH 和 SK-N-BE 细胞，建立 MPP 刺激的 PD 细胞模型，检测 MALAT1 的表达。然后，在 MPP 刺激的 PD 细胞模型中，检测 MALAT1 耗竭对细胞增殖和凋亡的影响。此外，还探讨了 MPP 刺激的 PD 细胞模型中 MALAT1 与 microRNA-135b-5p（miR-135b-5p）或糖蛋白非转移性黑色素瘤蛋白 B（GPNMB）之间的相关性。

结果

MALAT1 表达增加，下调 MALAT1 促进 MPP 刺激的细胞增殖，抑制细胞凋亡。此外，miR-135b-5p 是 MALAT1 的靶基因，可直接靶向 GPNMB。进一步研究表明，抑制 MALAT1 通过 miR-135b-5p/GPNMB 轴调节细胞增殖和凋亡。

结论

我们的研究结果表明，MALAT1/miR-135b-5p/GPNMB 轴调节 MPP 刺激的 PD 细胞模型中的细胞增殖和凋亡，为 PD 提供了一个潜在的生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/3b9ac8ca6f25/40659_2021_332_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/8f1b426b7813/40659_2021_332_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/9bcc6f6043b2/40659_2021_332_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/8a6aaabf3dec/40659_2021_332_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/0aa293d1ae59/40659_2021_332_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/98b303ad4cdd/40659_2021_332_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/3b9ac8ca6f25/40659_2021_332_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/8f1b426b7813/40659_2021_332_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/9bcc6f6043b2/40659_2021_332_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/8a6aaabf3dec/40659_2021_332_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/0aa293d1ae59/40659_2021_332_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/98b303ad4cdd/40659_2021_332_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a33/7968316/3b9ac8ca6f25/40659_2021_332_Fig6_HTML.jpg

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LncRNA MALAT1 facilitates inflammasome activation via epigenetic suppression of Nrf2 in Parkinson's disease.长链非编码 RNA MALAT1 通过表观遗传抑制 Nrf2 促进帕金森病中的炎症小体激活。
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