IL-17可轻度修复LCN2过表达引起的肺泡上皮细胞增殖障碍

IF 2.1 4区 医学 Q3 RESPIRATORY SYSTEM
Canadian respiratory journal Pub Date : 2024-08-06 eCollection Date: 2024-01-01 DOI:10.1155/2024/9284430
Tingting Lv, Ziliang Hou, Kaiyuan Yang, Jinxiang Wang
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引用次数: 0

摘要

导言:肺泡上皮细胞损伤后增殖能力受损是导致上皮修复功能障碍的一个重要因素,从而导致特发性肺纤维化(IPF)的发生。肺泡2型(AT2)细胞作为肺泡上皮的干细胞,参与了肺泡损伤后的修复过程。脂褐素-2(LCN2)参与调节肺泡上皮细胞病理过程的多个过程,但其机制尚不清楚:方法:我们利用BLM处理的小鼠模型研究了LCN2在肺纤维化区域的表达特征,并分析了LCN2在肺泡上皮细胞中的位置。此外,在体外用 LCN2 过表达质粒载体转染人肺泡上皮细胞(HPAEpiCs)。给 HPAEpiCs 注射不同浓度的重组人白细胞介素-17(IL-17)蛋白(rhIL-17),观察细胞活力并分析 IL-17 的浓度依赖效应:结果:BLM损伤后肺泡上皮细胞中LCN2增高,高表达的LCN2主要集中在BLM损伤肺的AT2细胞上。同时,LCN2-表达缺失的HPAEpiC细胞显示出细胞活力和细胞生长受损。用rhIL-17干预HPAEpiC可轻度挽救LCN2过表达引起的细胞增殖受损,且IL-17干预的效果部分取决于浓度:结果表明,IL-17对LCN2过表达导致的肺泡上皮细胞增殖能力受损具有逆转作用。该过程调控的靶肺泡上皮细胞是AT2细胞,为肺泡上皮损伤后的修复和肺损伤疾病的治疗提供了新的线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IL-17 Mildly Rescued the Impaired Proliferation of Alveolar Epithelial Cells Induced by LCN2 Overexpression.

Introduction: The impaired proliferative capacity of alveolar epithelial cells after injury is an important factor causing epithelial repair dysfunction, leading to the occurrence of idiopathic pulmonary fibrosis (IPF). Alveolar type 2 (AT2) cells as the stem cells of alveolar epithelium participate in the repair process after alveolar injury. Lipocalin-2 (LCN2) participates in multiple processes regulating the pathological process of alveolar epithelial cells, but the mechanisms involved are still unclear.

Method: We used a BLM-treated mouse model to characterize the expression of LCN2 in lung fibrosis regions and analyzed the location of LCN2 in alveolar epithelial cells. Moreover, human pulmonary alveolar epithelial cells (HPAEpiCs) were transfected with the LCN2 overexpression plasmid vector in vitro. Recombinant human interleukin-17 (IL-17) protein (rhIL-17) at different concentrations was administered to intervene in HPAEpiCs, observing cell viability and analyzing the concentration-dependent effect of IL-17.

Results: LCN2 was increased in the alveolar epithelium post-BLM injury, and highly expressed LCN2 was mainly concentrated on AT2 cells in BLM-injured lungs. Meanwhile, LCN2-overexpressing HPAEpiCs showed impaired cell viability and cell growth. HPAEpiC intervention with rhIL-17 mildly rescued the impaired cell proliferation induced by LCN2 overexpression, and the effect of IL-17 intervention was partially concentration-dependent.

Conclusions: The results revealed the reversed effect of IL-17 on the impaired proliferative capacity of the alveolar epithelium induced by LCN2 overexpression. The target alveolar epithelial cells regulated by this process were AT2 cells, providing new clues for alveolar epithelium repair after injury and the treatment of lung injury diseases.

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来源期刊
Canadian respiratory journal
Canadian respiratory journal 医学-呼吸系统
CiteScore
4.20
自引率
0.00%
发文量
61
审稿时长
6-12 weeks
期刊介绍: Canadian Respiratory Journal is a peer-reviewed, Open Access journal that aims to provide a multidisciplinary forum for research in all areas of respiratory medicine. The journal publishes original research articles, review articles, and clinical studies related to asthma, allergy, COPD, non-invasive ventilation, therapeutic intervention, lung cancer, airway and lung infections, as well as any other respiratory diseases.
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