Interleukin-19 Aggravates Pulmonary Fibrosis via Activating Fibroblast through TGF-β/Smad Pathway.
Interleukin-19 Aggravates Pulmonary Fibrosis via Activating Fibroblast through TGF-β/Smad Pathway.
复制标题
Interleukin-19 通过 TGF-β/Smad 途径激活成纤维细胞加重肺纤维化
DOI：
10.1155/2022/6755407
复制
发表时间：
2022
影响因子：
4.6
通讯作者：
Wu J
中科院分区：
文献类型：
--
作者：
Wang Y;Sun S;Wang K;Zhang M;Li M;Zan Y;Huang Q;Wu S;Zhao W;Xu W;Wu J
特发性肺纤维化（IPF）是一种无法治愈的进行性和致死性间质性肺炎疾病。受损细胞之间的通信是由细胞因子及其受体的复杂网络触发和维持的。越来越多的证据支持IL-19在呼吸系统疾病中的有害作用。然而，其在肺纤维化中的潜在作用从未被探索过。 采用生物信息学、免疫组化和Western blot分析方法检测IL-19在人和小鼠肺纤维化组织中的表达。采用CCK-8法、transwell法和流式细胞术分析IL-19对肺成纤维细胞生物学行为的影响。组织学用于阐明IL-19在体内的促纤维化作用。 IL-19在纤维化肺组织中上调。IL-19促进肺成纤维细胞增殖和侵袭，抑制细胞凋亡，诱导成纤维细胞向肌成纤维细胞分化，TGF-β/Smad信号通路抑制剂LY2109761可逆转IL-19的作用。此外，我们发现IL-19加重博莱霉素诱导的小鼠肺纤维化中的肺纤维化。 我们的研究结果暗示了IL-19通过直接作用于肺成纤维细胞的促纤维化作用以及靶向IL-19用于肺纤维化治疗干预的潜力。
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial pneumonia disease with no cure. Communication between injured cells is triggered and maintained by a complicated network of cytokines and their receptors. IL-19 is supported by increasing evidences for a deleterious role in respiratory diseases. However, its potential role in lung fibrosis has never been explored. Bioinformatic, immunohistochemistry and western blot analysis were used to assess the expression of IL-19 in human and mouse fibrosis lung tissues. CCK-8, transwell and flow cytometry assay were utilized to analyze the effect of IL-19 on biological behaviors of lung fibroblasts. Histopathology was used to elucidate profibrotic effect of IL-19 in vivo. IL-19 was upregulated in fibrosis lung tissues. IL-19 promoted lung fibroblasts proliferation and invasion, inhibited cell apoptosis, and induced differentiation of fibroblasts to the myofibroblast phenotype, which could be revised by LY2109761, a TGF-β/Smad signaling pathway inhibitor. Furthermore, we found that IL-19 aggravated lung fibrosis in murine bleomycin-induced lung fibrosis. Our results imply the profibrotic role for IL-19 through direct effects on lung fibroblasts and the potential of targeting IL-19 for therapeutic intervention in pulmonary fibrosis.
登录
查看更多内容
影响因子：
7.3
作者：
Niess JH;Hruz P;Kaymak T
通讯作者：
Kaymak T
影响因子：
7.3
作者：
Kragstrup TW;Andersen T;Heftdal LD;Hvid M;Gerwien J;Sivakumar P;Taylor PC;Senolt L;Deleuran B
通讯作者：
Deleuran B
DOI：
10.1007/978-1-4939-8570-8_5
发表时间：
2018-01-01
期刊：
LUNG INNATE IMMUNITY AND INFLAMMATION: METHODS AND PROTOCOLS
影响因子：
--
作者：
Edelman, Benjamin L.;Redente, Elizabeth F.
通讯作者：
Redente, Elizabeth F.
影响因子：
7.3
作者：
Autieri MV
通讯作者：
Autieri MV
影响因子：
10.6
作者：
Chanda D;Otoupalova E;Smith SR;Volckaert T;De Langhe SP;Thannickal VJ
通讯作者：
Thannickal VJ