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已发表论文
miR-335-5p 预示慢性阻塞性肺疾病（COPD）易感性升高及其在人支气管上皮细胞损伤中的作用
Received 15 January 2025
Accepted for publication 29 June 2025
Published 26 September 2025 Volume 2025:20 Pages 3317—3326
DOI https://doi.org/10.2147/COPD.S517725
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Richard Russell
Yifeng Zheng, Zhi Wu, Li Lin
Department of Respiratory and Critical Care Medicine, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou, Fujian, 363000, People’s Republic of China
Correspondence: Li Lin, Department of Respiratory and Critical Care Medicine, Zhangzhou Affiliated Hospital of Fujian Medical University, No. 59, Shengli Road, Zhangzhou, Fujian, 363000, People’s Republic of China, Tel +86-0596-2082950, Email LinliFJ67@163.com
Purpose: Chronic obstructive pulmonary disease (COPD) suffers from high prevalence, disability and mortality rates and a heavy economic burden. miR-335-5p takes part in multiple respiratory diseases such as pulmonary fibrosis, whereas its study in COPD has not been reported. The aim of our research was to explore miR-335-5p in predicting elevated COPD susceptibility and in human bronchial epithelial cells injury.
Patients and Methods: qRT-PCR was performed to examine miR-335-5p levels in serum and cells. ROC curve and logistic regression analyses were utilized to evaluate the predictive capacity of miR-335-5p for COPD susceptibility. Pearson correlation was used to assess the association of miR-335-5p with TNF-α, IL-6, FEV1, and FEV1/FVC. Human bronchial epithelial cells were exposed to cigarette smoke extract (CSE) conditions to simulate cell injury. Cell proliferation, apoptosis, inflammatory response and oxidative stress-related factors were assayed by CCK8, flow cytometry and ELISA, respectively.
Results: miR-335-5p is reduced on COPD patients. ROC curve recommended that miR-335-5p has high sensitivity (88.9%) and specificity (80.0%) to distinguish COPD from healthy individuals. Logistic regression showed that reduced miR-335-5p predicted elevated COPD susceptibility. Moreover, miR-335-5p was significantly negatively related to TNF-α and IL-6 and positively related to FEV1, and FEV1/FVC in COPD patients. Cellular experiments revealed that CSE treatment decreased miR-335-5p expression, repressed cell proliferation, facilitated apoptosis, raised TNF-α, IL-6, ROS, and MDA levels, and reduced SOD levels. miR-335-5p overexpression facilitated cell proliferation, suppressed apoptosis, diminished TNF-α, IL-6, ROS, and MDA levels, and elevated SOD levels, whereas knockdown of miR-335-5p reversed this trend.
Conclusion: Downregulation of miR-335-5p increased COPD susceptibility and negatively correlated with inflammatory factors. Overexpression of miR-335-5p alleviated CSE-induced injury to human bronchial epithelial cells, which suggested that miR-335-5p may be a potential target for COPD treatment.
Keywords: chronic obstructive pulmonary disease, susceptibility, human bronchial epithelial cells, miR-335-5p
Department of Respiratory and Critical Care Medicine, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou, Fujian, 363000, People’s Republic of China
Correspondence: Li Lin, Department of Respiratory and Critical Care Medicine, Zhangzhou Affiliated Hospital of Fujian Medical University, No. 59, Shengli Road, Zhangzhou, Fujian, 363000, People’s Republic of China, Tel +86-0596-2082950, Email LinliFJ67@163.com
Purpose: Chronic obstructive pulmonary disease (COPD) suffers from high prevalence, disability and mortality rates and a heavy economic burden. miR-335-5p takes part in multiple respiratory diseases such as pulmonary fibrosis, whereas its study in COPD has not been reported. The aim of our research was to explore miR-335-5p in predicting elevated COPD susceptibility and in human bronchial epithelial cells injury.
Patients and Methods: qRT-PCR was performed to examine miR-335-5p levels in serum and cells. ROC curve and logistic regression analyses were utilized to evaluate the predictive capacity of miR-335-5p for COPD susceptibility. Pearson correlation was used to assess the association of miR-335-5p with TNF-α, IL-6, FEV1, and FEV1/FVC. Human bronchial epithelial cells were exposed to cigarette smoke extract (CSE) conditions to simulate cell injury. Cell proliferation, apoptosis, inflammatory response and oxidative stress-related factors were assayed by CCK8, flow cytometry and ELISA, respectively.
Results: miR-335-5p is reduced on COPD patients. ROC curve recommended that miR-335-5p has high sensitivity (88.9%) and specificity (80.0%) to distinguish COPD from healthy individuals. Logistic regression showed that reduced miR-335-5p predicted elevated COPD susceptibility. Moreover, miR-335-5p was significantly negatively related to TNF-α and IL-6 and positively related to FEV1, and FEV1/FVC in COPD patients. Cellular experiments revealed that CSE treatment decreased miR-335-5p expression, repressed cell proliferation, facilitated apoptosis, raised TNF-α, IL-6, ROS, and MDA levels, and reduced SOD levels. miR-335-5p overexpression facilitated cell proliferation, suppressed apoptosis, diminished TNF-α, IL-6, ROS, and MDA levels, and elevated SOD levels, whereas knockdown of miR-335-5p reversed this trend.
Conclusion: Downregulation of miR-335-5p increased COPD susceptibility and negatively correlated with inflammatory factors. Overexpression of miR-335-5p alleviated CSE-induced injury to human bronchial epithelial cells, which suggested that miR-335-5p may be a potential target for COPD treatment.
Keywords: chronic obstructive pulmonary disease, susceptibility, human bronchial epithelial cells, miR-335-5p