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lncRNA-p21/AIF-1/CMPK2/NLRP3 通路通过外泌体促进尿酸诱导的人肾小管上皮细胞炎症、自噬和凋亡。

LincRNA-p21/AIF-1/CMPK2/NLRP3 pathway promoted inflammation, autophagy and apoptosis of human tubular epithelial cell induced by urate via exosomes.

机构信息

Department of Nephrology, Southern University of Science and Technology Hospital, Shenzhen, China.

出版信息

Sci Rep. 2024 Aug 5;14(1):18146. doi: 10.1038/s41598-024-69323-5.

DOI:10.1038/s41598-024-69323-5
PMID:39103417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11300820/
Abstract

Urate nephropathy, a common complication of hyperuricemia, has garnered increasing attention worldwide. However, the exact pathogenesis of this condition remains unclear. Currently, inflammation is widely accepted as the key factor in urate nephropathy. Therefore, the aim of this study was to elucidate the interaction of lincRNA-p21/AIF-1/CMPK2/NLRP3 via exosomes in urate nephropathy. This study evaluated the effect of lincRNA-p21/AIF-1/CMPK2/NLRP3 using clinical data collected from patients with urate nephropathy and human renal tubular epithelial cells (HK2) cultured with different concentrations of urate. In clinical research section, the level of lincRNA-p21/AIF-1 in exosomes of urine in patients with hyperuricemia or urate nephropathy was found to be increased, particularly in patients with urate nephropathy. In vitro study section, the level of exosomes, inflammation, autophagy, and apoptosis was increased in HK2 cells induced by urate. Additionally, the expression of lincRNA-p21, AIF-1, CMPK2, and NLRP3 was upregulated in exosomes and HK2 cells. Furthermore, manipulating the activity of lincRNA-p21, AIF-1, CMPK2, and NLRP3 through overexpression or interference vectors regulated the level of inflammation, autophagy, and apoptosis in HK2 cells. In conclusion, the pathway of lincRNA-p21/AIF-1/CMPK2/NLRP3 contributed to inflammation, autophagy, and apoptosis of human renal tubular epithelial cell induced by urate via exosomes. Additionally, the specific exosomes in urine might serve as novel biomarkers for urate nephropathy.

摘要

尿酸肾病是高尿酸血症的常见并发症，已引起全球越来越多的关注。然而，这种疾病的确切发病机制尚不清楚。目前，炎症被广泛认为是尿酸肾病的关键因素。因此，本研究旨在阐明 lincRNA-p21/AIF-1/CMPK2/NLRP3 通过外泌体在尿酸肾病中的相互作用。本研究通过收集尿酸肾病患者的临床数据和不同浓度尿酸培养的人肾小管上皮细胞（HK2），评估了 lincRNA-p21/AIF-1/CMPK2/NLRP3 的作用。在临床研究部分，发现高尿酸血症或尿酸肾病患者尿液外泌体中的 lincRNA-p21/AIF-1 水平升高，特别是尿酸肾病患者。在体外研究部分，尿酸诱导的 HK2 细胞中外泌体、炎症、自噬和细胞凋亡水平增加，外泌体和 HK2 细胞中 lincRNA-p21、AIF-1、CMPK2 和 NLRP3 的表达上调。此外，通过过表达或干扰载体操纵 lincRNA-p21、AIF-1、CMPK2 和 NLRP3 的活性，调节 HK2 细胞中炎症、自噬和细胞凋亡的水平。总之，lincRNA-p21/AIF-1/CMPK2/NLRP3 通路通过外泌体促进尿酸诱导的人肾小管上皮细胞的炎症、自噬和细胞凋亡，并且尿液中的特定外泌体可能作为尿酸肾病的新型生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/8d4637dbb5d7/41598_2024_69323_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/1397a6c452bc/41598_2024_69323_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/e84c5c9e89dd/41598_2024_69323_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/630be4823c33/41598_2024_69323_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/787b69026de8/41598_2024_69323_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/5144d416832d/41598_2024_69323_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/3b0f10018e85/41598_2024_69323_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/8d4637dbb5d7/41598_2024_69323_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/1397a6c452bc/41598_2024_69323_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/e84c5c9e89dd/41598_2024_69323_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/630be4823c33/41598_2024_69323_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/787b69026de8/41598_2024_69323_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/5144d416832d/41598_2024_69323_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/3b0f10018e85/41598_2024_69323_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/badc/11300820/8d4637dbb5d7/41598_2024_69323_Fig7_HTML.jpg

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LincRNA-p21/AIF-1/CMPK2/NLRP3 pathway promoted inflammation, autophagy and apoptosis of human tubular epithelial cell induced by urate via exosomes.

Sci Rep. 2024-8-5

[2]
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[3]
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[4]
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[5]
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[6]
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[10]
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[2]
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[3]
Control of Cell Death in Health and Disease.

Annu Rev Pathol. 2024-1-24

[4]
Clinical and pathological correlation between urinary exosome miR-223 and IgAN patients.

Clin Nephrol. 2023-11

[5]
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Exp Mol Med. 2023-8

[6]
Endothelial Gata6 deletion reduces monocyte recruitment and proinflammatory macrophage formation and attenuates atherosclerosis through Cmpk2-Nlrp3 pathways.

Redox Biol. 2023-8

[7]
A 360° view of the inflammasome: Mechanisms of activation, cell death, and diseases.

Cell. 2023-5-25

[8]
Serum Urate and Risk of Chronic Kidney Disease: A Mendelian Randomization Study Using Taiwan Biobank.

Mayo Clin Proc. 2023-4

[9]
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Front Immunol. 2023

[10]
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