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Annexin A1 is elevated in patients with COPD and affects lung fibroblast function.

ABSTRACT: Fibrosis in peripheral airways is responsible for airflow limitation in chronic obstructive pulmonary disease (COPD). Annexin A1 modulates several key biological events during inflammation. However, little is known about its role in airway fibrosis in COPD. We investigated whether levels of Annexin A1 were upregulated in patients with COPD, and whether it promoted airway fibrosis.We quantified serum Annexin A1 levels in never-smokers (n=12), smokers without COPD (n=11), and smokers with COPD (n=22). Correlations between Annexin A1 expression and clinical indicators (eg, lung function) were assessed. In vitro, human bronchial epithelial (HBE) cells were exposed to cigarette smoke extract (CSE) and Annexin A1 expression was assessed. Primary human lung fibroblasts were isolated from patients with COPD and effects of Annexin A1 on fibrotic deposition of lung fibroblasts were evaluated.Serum Annexin A1 was significantly higher in patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines stage III or IV than in those with GOLD stages I or II (12.8±0.8 ng/mL versus 9.8±0.7 ng/mL; p=0.016). Annexin A1 expression was negatively associated with airflow obstruction (forced expiratory volume in one second % predicted; r=-0.72, p<0.001). In vitro, Annexin A1 was significantly increased in CSE-exposed HBE cells in a time- and concentration-dependent manner. Annexin A1 promoted lung fibroblasts proliferation, migration, differentiation, and collagen deposition via the ERK1/2 and p38 mitogen-activated protein kinase pathways.Annexin A1 expression is upregulated in patients with COPD and affects lung fibroblast function. However, more studies are needed to clarify the role of Annexin A1 in airway fibrosis of COPD.

SUBMITTER: Lai T

PROVIDER: S-EPMC5804736 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Annexin A1 is elevated in patients with COPD and affects lung fibroblast function.

Lai Tianwen T Li Yanyu Y Mai Zongjiong Z Wen Xiaoxia X Lv Yingying Y Xie Zhanqing Z Lv Quanchao Q Chen Min M Wu Dong D Wu Bin B

International journal of chronic obstructive pulmonary disease 20180205

<h4>Purpose</h4>Fibrosis in peripheral airways is responsible for airflow limitation in chronic obstructive pulmonary disease (COPD). Annexin A1 modulates several key biological events during inflammation. However, little is known about its role in airway fibrosis in COPD. We investigated whether levels of Annexin A1 were upregulated in patients with COPD, and whether it promoted airway fibrosis.<h4>Methods</h4>We quantified serum Annexin A1 levels in never-smokers (n=12), smokers without COPD ( ...[more]

PMID: 29440885

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Project description:Background and Objective Annexin A1 (annexin I, ANXA1), the first discovered member of the annexin superfamily, plays important roles in tumor development, invasion, metastasis, apoptosis and drug resistance based on tumor type-specific patterns of expression. The acquisition of the epithelial-mesenchymal transition (EMT) characteristics is an essential mechanism of metastasis because they increase the mobility and invasiveness of cancer cells. Cancer invasion and metastasis remain major health problems worldwide. Elucidating the role and mechanism of ANXA1 in the occurrence of EMT will help advance the development of novel therapeutic strategies. Hence, this review aims to attract everyone’s attention to the important role of ANXA1 in tumors and provide new ideas for clinical tumor treatment. Methods The PubMed database was mainly used to search for various English research papers and reviews related to the role of ANXA1 in tumors and EMT published from November 1994 to April 2022. The search terms used mainly include ANXA1, EMT, tumor, cancer, carcinoma, and mechanism. Key Content and Findings This article mainly provides a summary of the roles of ANXA1 and EMT in tumor metastasis as well as the various mechanisms via which ANXA1 facilitates the occurrence of EMT, thereby affecting tumor metastasis. In addition, the expression of ANXA1 in different metastatic tumor cell lines and its roles in tumorigenesis and development are also elaborated. This article has found many tumorous therapeutic targets related to ANXA1 and EMT, further confirming that ANXA1 has a huge potential for the diagnosis, treatment and prognosis of certain cancers. Conclusions Both the abnormal expression of ANXA1 and the occurrence of EMT are closely related to the invasion and metastasis of tumors, and more interestingly, ANXA1 can impact EMT directly or indirectly by mediating signaling pathways and adhesion among cells. We need more studies to elucidate the effects of ANXA1 on tumor invasion, migration and metastasis through EMT in vitro and in vivo clearly, and ultimately in patients to identify more therapeutic targets.

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Annexin A1 is elevated in patients with COPD and affects lung fibroblast function.

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Annexin A1 is elevated in patients with COPD and affects lung fibroblast function.

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