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miR-31-5p 作为慢性炎症性脱髓鞘性多发性神经病临床改善的潜在循环生物标志物和示踪剂。

miR-31-5p as a Potential Circulating Biomarker and Tracer of Clinical Improvement for Chronic Inflammatory Demyelinating Polyneuropathy.

机构信息

Department of Neurology, Wroclaw Medical University, Borowska 213, 50-556 Wroclaw, Poland.

Department of Molecular and Cellular Biology, Wroclaw Medical University, Borowska 211A, Wroclaw, Poland.

出版信息

Oxid Med Cell Longev. 2023 Apr 10;2023:2305163. doi: 10.1155/2023/2305163. eCollection 2023.

DOI:10.1155/2023/2305163
PMID:37077658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10110370/
Abstract

BACKGROUND

MicroRNAs are endogenous, small noncoding RNA molecules that play a pivotal role in the regulation of gene expression. MicroRNAs are involved in many biological processes such as proliferation, cell differentiation, neovascularization, and apoptosis. Studies on microRNA expression may contribute to a better understanding of the pathomechanism of chronic inflammatory demyelinating polyneuropathy (CIDP) and consequently enable the development of new therapeutic measures using antisense miRNAs (antagomirs). In this study, we evaluated the level of miR-31-5p in the serum of patients with CIDP and its correlation with the miR-31-5p level and clinical presentation and electrophysiological and biochemical parameters.

METHODS

The study group consisted of 48 patients, mean age 61.60 ± 11.76, who fulfilled the diagnostic criteria of a typical variant of CIDP. The expression of miR-31-5p in patient serum probes was investigated by droplet digital PCR. The results were correlated with neurophysiological findings and the patient's clinical and biochemical parameters.

RESULTS

The mean copy number of miRNA-31 in 100 l serum was 1288.64 ± 2001.02 in the CIDP group of patients, while in the control group, it was 3743.09 ± 4026.90. There was a significant positive correlation (0.426) between IgIV treatment duration and miR-31-5p expression. Patients without IgIV treatment showed significantly lower levels of miR-31 compared to the treated group (259.44 ± 304.02 vs. 1559.48 ± 2168.45; = 0.002). The group of patients with body weight > 80 kg showed statistically significantly lower levels of miRNA-31-5p than the patients with lower body weight (934.37 ± 1739.66 vs. 1784.62 ± 2271.62, respectively; = 0.014). Similarly, the patients with elevated cerebrospinal fluid (CSF) protein levels had significantly higher miRNA-31-5p expression than those with normal protein levels (1393.93 ± 1932.27 vs. 987.38 ± 2364.10, respectively; = 0.044).

CONCLUSION

The results may support the hypothesis that miR-31-5p is strongly involved in the autoimmune process in CIDP. The positive correlation between higher miR-31-5p levels and duration of IVIg treatment may be an additional factor explaining the efficacy of prolonged IVIg therapy in CIDP.

摘要

背景

MicroRNAs 是内源性的小非编码 RNA 分子,在基因表达调控中起着关键作用。MicroRNAs 参与许多生物学过程,如增殖、细胞分化、新生血管形成和细胞凋亡。MicroRNA 表达的研究可能有助于更好地理解慢性炎症性脱髓鞘性多发性神经病 (CIDP) 的发病机制,并因此能够利用反义 miRNA(antagomirs)开发新的治疗措施。在这项研究中,我们评估了 CIDP 患者血清中 miR-31-5p 的水平及其与 miR-31-5p 水平以及临床表现、电生理和生化参数的相关性。

方法

研究组包括 48 名患者,平均年龄 61.60 ± 11.76 岁,符合 CIDP 典型变异的诊断标准。通过液滴数字 PCR 研究患者血清探针中 miR-31-5p 的表达。结果与神经生理学发现以及患者的临床和生化参数相关联。

结果

CIDP 组患者 100μl 血清中 miRNA-31 的平均拷贝数为 1288.64 ± 2001.02,而对照组为 3743.09 ± 4026.90。miR-31-5p 表达与 IgGIV 治疗持续时间呈显著正相关(0.426)。未接受 IgGIV 治疗的患者的 miR-31 水平明显低于治疗组(259.44 ± 304.02 vs. 1559.48 ± 2168.45; = 0.002)。体重>80kg 的患者组的 miRNA-31-5p 水平明显低于体重较低的患者组(934.37 ± 1739.66 vs. 1784.62 ± 2271.62,分别; = 0.014)。同样,脑脊液(CSF)蛋白水平升高的患者的 miR-31-5p 表达明显高于蛋白水平正常的患者(1393.93 ± 1932.27 vs. 987.38 ± 2364.10,分别; = 0.044)。

结论

结果可能支持 miR-31-5p 强烈参与 CIDP 自身免疫过程的假说。较高的 miR-31-5p 水平与 IVIg 治疗持续时间之间的正相关可能是解释 IVIg 延长治疗在 CIDP 中有效性的另一个因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/42d6d55d8205/OMCL2023-2305163.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/2cd7a57112c4/OMCL2023-2305163.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/577a501aa3a2/OMCL2023-2305163.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/42d6d55d8205/OMCL2023-2305163.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/2cd7a57112c4/OMCL2023-2305163.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/577a501aa3a2/OMCL2023-2305163.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4a/10110370/42d6d55d8205/OMCL2023-2305163.003.jpg

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