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Title: Effects of microRNA-21 on endothelial-to-mesenchymal transition and its role in the pathogenesis of chronic obstructive pulmonary disease.
Author: Liao Y, Zeng Z, Cai J, Sun S, Xie L.
Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2023 Mar 28; 48(3):323-329. PubMed ID: 37164915.
Abstract:
OBJECTIVES: Chronic obstructive pulmonary disease (COPD) is a disease characterized by persistent airflow restriction. This study aims to explore whether there is endothelial-to-mesenchymal transition (EndMT) in COPD mice and to explore the relationship between microRNA-21 (miR-21) and EndMT. METHODS: We established the COPD and the miR-21 gene knockout COPD animal model (both cigarette smoke-induced). Mice were divided into 3 groups (n=4): a control group, a COPD group, and a miR-21 knockout COPD (miR-21^-/^--COPD) group. Masson trichrome staining was used to observe the deposition of collagen around the perivascular. The relative protein levels and positions of endothelial cell markers including vascular endothelial-cadherin (VE-cadherin), endothelial nitric oxide synthase (eNOS), and platelet endothelial cell adhesion molecule-1 (CD31) as well as mesenchymal cell markers including α-smooth muscle actin (α-SMA) and neural cadherin (N-cadherin) in lung tissues were observed by immunohistochemical staining. RESULTS: Compared with the control group, the area of collagen fibril deposition was increased in the COPD group (P<0.05), the expression levels of VE-cadherin, eNOS, and CD31 were all decreased (all P<0.05), and the expression levels of α-SMA and N-cadherin were increased (both P<0.05). Compared with the COPD group, the miR-21^-/^--COPD group had a reduced area of collagen fiber deposition (P<0.05), the expression levels of VE-cadherin, eNOS, and CD31 were all increased (all P<0.05), and the expression levels of α-SMA and N-cadherin were decreased (both P<0.05). CONCLUSIONS: There is a EndMT process in cigarette smoke-induced COPD animal models.MiR-21 gene knockdown could reduce collagen deposition area and inhibit the EndMT process in COPD mice. 目的: 慢性阻塞性肺疾病(chronic obstructive pulmonary disease，COPD)是一种以持续气流受限为特征的疾病。本研究旨在探讨COPD小鼠模型是否存在内皮-间充质转化(endothelial-to-mesenchymal transition，EndMT)，并初步探讨微RNA(microRNA，miR)-21与EndMT的关系。方法: 建立小鼠COPD模型及miR-21基因敲除COPD动物模型(均为香烟烟雾诱导)，将小鼠分为3组(n=4)：对照组、COPD组和miR-21基因敲除COPD组(miR-21^-/^--COPD组)。采用Masson三色染色法观察血管周围胶原纤维沉积的情况，免疫组织化学染色观察肺组织切片中内皮细胞标志物血管内皮钙黏蛋白(vascular endothelial-cadherin，VE-cadherin)、内皮一氧化氮合酶(endothelial nitric oxide synthase，eNOS)、血小板内皮细胞黏附分子-1(platelet endothelial cell adhesion molecule-1，CD31)和间皮细胞标志物α-平滑肌肌动蛋白(α-smooth muscle actin，α-SMA)、神经钙黏蛋白(neural cadherin，N-cadherin)的表达情况。结果: 与对照组相比，COPD组的胶原纤维沉积面积增加(P<0.05)，VE-cadherin、eNOS、CD31的表达水平降低(均P<0.05)，α-SMA、N-cadherin表达水平均升高(均P<0.05)。与COPD组相比，miR-21^-/^--COPD组胶原纤维沉积面积减小(P<0.05)，VE-cadherin、eNOS、CD31的表达水平均升高(均P<0.05)，α-SMA、N-cadherin表达水平均降低(均P<0.05)。结论: 香烟烟雾诱导的COPD动物模型存在EndMT过程，miR-21基因敲除可减少COPD小鼠血管周围胶原纤维沉积面积和延缓EndMT过程。. OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is a disease characterized by persistent airflow restriction. This study aims to explore whether there is endothelial-to-mesenchymal transition (EndMT) in COPD mice and to explore the relationship between microRNA-21 (miR-21) and EndMT. METHODS: We established the COPD and the miR-21 gene knockout COPD animal model (both cigarette smoke-induced). Mice were divided into 3 groups (n=4): a control group, a COPD group, and a miR-21 knockout COPD (miR-21^-/^--COPD) group. Masson trichrome staining was used to observe the deposition of collagen around the perivascular. The relative protein levels and positions of endothelial cell markers including vascular endothelial-cadherin (VE-cadherin), endothelial nitric oxide synthase (eNOS), and platelet endothelial cell adhesion molecule-1 (CD31) as well as mesenchymal cell markers including α-smooth muscle actin (α-SMA) and neural cadherin (N-cadherin) in lung tissues were observed by immunohistochemical staining. RESULTS: Compared with the control group, the area of collagen fibril deposition was increased in the COPD group (P<0.05), the expression levels of VE-cadherin, eNOS, and CD31 were all decreased (all P<0.05), and the expression levels of α-SMA and N-cadherin were increased (both P<0.05). Compared with the COPD group, the miR-21^-/^--COPD group had a reduced area of collagen fiber deposition (P<0.05), the expression levels of VE-cadherin, eNOS, and CD31 were all increased (all P<0.05), and the expression levels of α-SMA and N-cadherin were decreased (both P<0.05). CONCLUSION: There is a EndMT process in cigarette smoke-induced COPD animal models.MiR-21 gene knockdown could reduce collagen deposition area and inhibit the EndMT process in COPD mice.

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