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巨噬细胞相关的 microRNA-4715-3p/Gasdermin D 轴可能预示非酒精性脂肪性肝病纤维化进展：来自转录组和生物学数据的证据。

The macrophage-associated microRNA-4715-3p / Gasdermin D axis potentially indicates fibrosis progression in nonalcoholic fatty liver disease: evidence from transcriptome and biological data.

机构信息

Center of Gastrointestinal Disease, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, P.R. China.

Department of Hematology, Oncology and Tumor Immunology (CVK), Charité Universitätsmedizin Berlin, Berlin, Germany.

出版信息

Bioengineered. 2022 May;13(5):11740-11751. doi: 10.1080/21655979.2022.2072602.

DOI:10.1080/21655979.2022.2072602
PMID:35521691
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275955/
Abstract

Nonalcoholic fatty liver disease (NAFLD) is highly possible to progress to cirrhosis, malignancy, and liver failure through fibrogenesis. The enormous potential of pathogenetic and therapeutic targets in NAFLD has been revealed. This study aimed to explore novel factors potentially indicating or mediating NAFLD progression. Multiple bulk and single-cell RNA sequencing datasets were used, in which landscapes of cell populations were clarified to characterize immune cell infiltration. Significantly high infiltration of macrophages (MPs) was discovered during NAFLD progression. Samples in bulk NASH datasets were regrouped by MP level. Highly differentially expressed genes (DEGs) were identified in the Ctrl vs. NASH comparison, low MP vs. high MP comparison, and the weighted gene co-expression network analysis (WGCNA) clusters. Eight hub genes were identified as promising targets by protein-protein interaction analysis and validated in fibrosis progression, microRNA (miR)-protein interactions were predicted, and the hub genes were verified in a free fatty acid (FFA)-induced macrophage injury model. The results showed that Gasdermin D () was upregulated with fibrosis progression in NAFLD and was associated with macrophage infiltration. In addition, a potential regulator (miR-4715-3p) was correlated with . The miR-4715-3p/ axis potentially modulates macrophage-associated immunity and indicates fibrosis progression in NAFLD.

摘要

非酒精性脂肪性肝病 (NAFLD) 通过纤维化极有可能进展为肝硬化、恶性肿瘤和肝衰竭。NAFLD 的发病机制和治疗靶点具有巨大的潜力，这一点已经得到了揭示。本研究旨在探索可能预示或介导 NAFLD 进展的新因素。使用了多个批量和单细胞 RNA 测序数据集，其中阐明了细胞群体的景观以表征免疫细胞浸润。在 NAFLD 进展过程中发现巨噬细胞 (MP) 的浸润显著增加。批量 NASH 数据集的样本按 MP 水平重新分组。在 Ctrl 与 NASH 比较、低 MP 与高 MP 比较以及加权基因共表达网络分析 (WGCNA) 聚类中鉴定出高度差异表达基因 (DEG)。通过蛋白质-蛋白质相互作用分析鉴定了 8 个作为有前途的靶标的枢纽基因，并在纤维化进展中进行了验证，预测了 microRNA (miR)-蛋白质相互作用，并在游离脂肪酸 (FFA) 诱导的巨噬细胞损伤模型中验证了枢纽基因。结果表明，Gasdermin D () 在 NAFLD 纤维化进展中上调，与巨噬细胞浸润有关。此外，一个潜在的调节剂 (miR-4715-3p) 与 相关。miR-4715-3p/ 轴可能调节与巨噬细胞相关的免疫，并预示着 NAFLD 的纤维化进展。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f10a/9275955/ca84935cda7a/KBIE_A_2072602_F0006_OC.jpg

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