Endothelial Microparticles Derived from Primary Pulmonary Microvascular Endothelial Cells Mediate Lung Inflammation in Chronic Obstructive Pulmonary Disease by Transferring microRNA-126

He, Xue; Liu, Xiangming; Long, Yingjiao; Chen, Yan

doi:10.2147/jir.s349818

Cited by 7 publications

(6 citation statements)

References 61 publications

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“…Endothelial microparticles derived from endothelial cells can reduce the expression of HMGB1 in epithelial cells. This downregulated the release of TNF‐α and IL‐1β and then attenuated CSE‐induced inflammation in HBE cells 117 . The expression level of miR‐181a‐5p was lower in the lung tissues of COPD model mice.…”

Section: Inhibition or Blockade Of Hmgb1 Rage And Tlr4 As A Potential...mentioning

confidence: 88%

“…This downregulated the release of TNF-α and IL-1β and then attenuated CSEinduced inflammation in HBE cells. 117 The expression level of miR-181a-5p was lower in the lung tissues of COPD model mice. However, miR-181a-5p overexpression targets HMGB1 to inhibit the NF-κB pathway, thus alleviating the inflammatory response in COPD mice.…”

Section: Effects Of Hmgb1 Inhibition Against Copd Inflammationmentioning

confidence: 94%

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The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke‐induced inflammation in chronic obstructive pulmonary disease

Lin

Song

et al. 2022

Immunity Inflam & Disease

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Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease with irreversible and continuous progression. It has become the fifth most burdensome disease and the third most deadly disease globally. Therefore, the prevention and treatment of COPD are urgent, and it is also important to clarify the pathogenesis of it. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) can cause lung inflammation and other pathological mechanisms in the airways and lung tissue. Airway inflammation is one of the important mechanisms leading to the pathogenesis of COPD. Recent studies have shown that high mobility group box 1 (HMGB1) is involved in the occurrence and development of respiratory diseases, including COPD. HMGB1 is a typical damage‐associated molecular pattern (DAMP) protein, which mainly exerts its activity by binding to the receptor for advanced glycation end products (RAGE) and toll‐like receptor 4 (TLR4) and further participate in the process of airway inflammation. Studies have shown that the abnormal expression of HMGB1, RAGE, and TLR4 are related to inflammation in COPD. Herein, we discuss the roles of HMGB1, RAGE, and TLR4 in CS/cigarette smoke extract‐induced inflammation in COPD, providing a new target for the diagnosis, treatment and prevention of COPD.

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Section: Inhibition or Blockade Of Hmgb1 Rage And Tlr4 As A Potential...mentioning

confidence: 88%

Section: Effects Of Hmgb1 Inhibition Against Copd Inflammationmentioning

confidence: 94%

The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke‐induced inflammation in chronic obstructive pulmonary disease

Lin

Song

et al. 2022

Immunity Inflam & Disease

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“…Several studies have reported the changes in miRNA expression in lung tissues obtained from COPD patients and animal models of COPD exposed to cigarette smoke 11 , 12 , 29 . Previous studies have demonstrated that miR-21 30 , miR-126 31 and miR-34a 28 play an important role in the pathogenesis and development of COPD. Our research group conducted microarray analysis of the lung tissues of CS and CSE exposure-induced emphysema mice and control mice and found that a few miRNAs were differentially expressed in the lung tissues of emphysema mice.…”

Section: Discussionmentioning

confidence: 99%

MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1

Lin,

Song,

Cheng

et al. 2023

Tob. Induc. Dis.

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INTRODUCTION Abnormal apoptosis of pulmonary microvascular endothelial cells (PMVECs) participates in the pathogenesis of COPD. Studies have shown that microRNAs (miRNAs) contribute to the pathogenesis of pulmonary diseases by regulating cell apoptosis. The present study aimed to investigate the effects of miR-216a in cigarette smoke extract (CSE)-induced apoptosis of PMVECs in COPD and explore the potential mechanisms. METHODS The emphysema model mice were treated with CSE and CS exposure. The expression of miR-216a and DNA methyltransferase 1 (DNMT1) was assessed in emphysema mice and COPD patients. The miR-216a mimic and Lenti-DNMT1 were transfected into PMVECs to identify the underlying mechanisms. The expression levels of miR-216a and DNMT1 were detected by real-time quantitative polymerase chain reaction (RT-qPCR) or Western blot. Moreover, cell apoptosis was examined by flow cytometry assays. RESULTS The results show that the expression of miR-216a was decreased, whereas the expression of DNMT1 was increased in the lung tissue of emphysema mice and COPD patients. In addition, the expression of miR-216a was significantly reduced in CSE-treated PMVECs, and the overexpression of miR-216a attenuated CSE-induced PMVEC apoptosis. Furthermore, the expression of DNMT1 was increased in the CSE-induced PMVECs and then was reduced after the overexpression of miR-216a in the CSE-stimulated PMVECs. Luciferase reporter assays confirmed the target reaction between miR-216a and DNMT1. Also, the overexpression of DNMT1 was able to reverse the anti-apoptotic effect of miR-216a in CSE-induced PMVECs. CONCLUSIONS The results indicate that miR-216a may play a crucial role in CSE-induced apoptosis by directly regulating its target gene DNMT1 in COPD. It provides insights into the function of MiR-216a/DNMT1 as a potential molecule in COPD.

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“…Finally, CSE was diluted to the concentration of 40% for intraperitoneal injection into mice. The injection details were established as reported previously 23 . The mice in the control group were given 0.3 mL/20 g PBS through intraperitoneal injection, and the mice in the CS exposure group were given 0.3 mL/20 g, 40% CSE through intraperitoneal injection on days 1, 12, and 23.…”

Section: Cs Exposure Plus Cse-induced Mouse Modelmentioning

confidence: 99%

LRG1 promotes the apoptosis of pulmonary microvascular endothelial cells through KLK10 in chronic obstructive pulmonary disease

Cheng,

Song,

Zhou

et al. 2024

Tob. Induc. Dis.

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INTRODUCTION Cigarette smoking is one of the most important causes of COPD and could induce the apoptosis of pulmonary microvascular endothelial cells (PMVECs). The conditional knockout of LRG1 from endothelial cells reduced emphysema in mice. However, the mechanism of the deletion of LRG1 from endothelial cells rescued by cigarette smoke (CS) induced emphysema remains unclear. This research aimed to demonstrate whether LRG1 promotes the apoptosis of PMVECs through KLK10 in COPD. METHODS Nineteen patients were divided into three groups: control non-COPD (n=7), smoker non-COPD (n=7), and COPD (n=5). The emphysema mouse model defined as the CS exposure group was induced by CS exposure plus cigarette smoke extract (CSE) intraperitoneal injection for 28 days. Primary PMVECs were isolated from the mouse by magnetic bead sorting method via CD31-Dynabeads. Apoptosis was detected by western blot and flow cytometry. RESULTS LRG1 was increased in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. KLK10 was over-expressed in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. LRG1 promoted apoptosis in PMVECs. LRG1 knockdown reversed CSE-induced apoptosis in PMVECs. The mRNA and protein expression of KLK10 were increased after over-expressed LRG1 in PMVECs isolated from mice. Similarly, both the mRNA and protein levels of KLK10 were decreased after LRG1 knockdown in PMVECs. The result of co-immunoprecipitation revealed a protein-protein interaction between LRG1 and KLK10 in PMVECs. KLK10 promoted apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. KLK10 knockdown could reverse CSE-induced apoptosis in PMVECs. CONCLUSIONS LRG1 promotes apoptosis via up-regulation of KLK10 in PMVECs isolated from mice. KLK10 promotes apoptosis via the down-regulation of Bcl-2/ Bax in PMVECs. There was a direct protein-protein interaction between LRG1 and KLK10 in PMVECs. Our novel findings provide insights into the understanding of LRG1/KLK10 function as a potential molecule in COPD.

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Endothelial Microparticles Derived from Primary Pulmonary Microvascular Endothelial Cells Mediate Lung Inflammation in Chronic Obstructive Pulmonary Disease by Transferring microRNA-126

Cited by 7 publications

References 61 publications

The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke‐induced inflammation in chronic obstructive pulmonary disease

The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke‐induced inflammation in chronic obstructive pulmonary disease

MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1

LRG1 promotes the apoptosis of pulmonary microvascular endothelial cells through KLK10 in chronic obstructive pulmonary disease

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