KLF2 attenuates bleomycin-induced pulmonary fibrosis and inflammation with regulation of AP-1

Shi, Jian; Zhou, Lean; Wang, Xiaosheng; Du, Junfeng; Jiang, Mingming; Zhan, Shaoqi; Han, Guangchao; Mai, Zhitao

doi:10.1016/j.bbrc.2017.10.114

Cited by 23 publications

(18 citation statements)

References 30 publications

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“…relieves bleomycin-induced pulmonary fibrosis and inflammation by the mediation of Activator protein-1 [34]. In this work, IL-1β abated the expression of KLF2, whereas montelukast treatment reversed the effect of IL-1β on ATDC5 cells in a concentration-dependent way.…”

Section: Resultsmentioning

confidence: 49%

Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2)

Wang

Ma³

2021

Bioengineered

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Section: Resultsmentioning

confidence: 49%

Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2)

Wang

Ma³

2021

Bioengineered

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“…After the occurrence of AMI, the left ventricular dysfunction and remodeling can be promoted by the sustained inflammatory responses. KLF2 has been found to regulate some key molecules or signaling involved in inflammation [30,31]. As a regulator of KLF2, miR-32-5p has been found to contribute to inflammatory responses in macrophages infected by Mycobacterium tuberculosis [18] and rats with neuropathic pain [19].…”

Section: Discussionmentioning

confidence: 99%

Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction

2020

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Background: MicroRNAs (miRNAs) have been investigated in various cardiovascular diseases. As a fatal disease, acute myocardial infarction (AMI) is a serious global health burden. The purpose of this study was to investigate the role of miR-32-5p in AMI patients and human umbilical vein endothelial cells (HUVECs) to explore novel diagnostic and therapeutic approaches for AMI. Methods: A target prediction tool miRanda and the luciferase activity assay were used to confirm the interaction of miR-32-5p with Kruppel-like factor 2 (KLF2). Effect of miR-32-5p on HUVECs viability was examined using CCK-8 assay. Serum miR-32-5p expression was measured using quantitative Real-Time PCR, and its correlation with myocardial damage and endothelial injury markers and pro-inflammatory cytokines was assessed. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic value of miR-32-5p in AMI patients.Results: miR-32-5p, as a direct regulator of KLF2, could suppress the cell proliferation of HUVECs. Serum miR-32-5p expression was elevated in AMI patients and positively correlated with the biomarker levels of myocardial damage and endothelial injury and pro-inflammatory cytokines. The area under the ROC curve for miR-32-5p was 0.949, indicating the relatively high diagnostic accuracy of miR-32-5p in AMI patients. Conclusion: The data of this study revealed that the increased serum miR-32-5p expression serves as a candidate diagnostic biomarker of AMI, and that miR-32-5p may be involved in the myocardial damage, endothelial injury and inflammatory responses of AMI by targeting KLF2, indicating the potential of miR-32-5p as a diagnostic biomarker and molecular target to improve the treatment of AMI.

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“…Although these results were solid evidence to support the inhibitory effect of HSYA on TNF-α induced inflammation and cell proliferation of FB, the specific mechanism, however, is far from illustrated. TGF-β1 is deemed as the major profibrotic cytokine, and numerous studies have confirmed its critical role in the treatment of fibrotic diseases [20]. Transcription of TGF-β1 gene is dependent on transcription factor activator protein-1 (AP-1), and the study has confirmed that TNF-α promotes the expression of TGF-β1 in FB by activating AP-1 [21,22].…”

Section: Discussionmentioning

confidence: 99%

Hydroxysafflor Yellow A Inhibits TNF-α-Induced Inflammation of Human Fetal Lung Fibroblasts via NF-κB Signaling Pathway

Liu

Wang

Wen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Objective. Hydroxysafflor yellow A (HSYA), an effective ingredient of the Chinese herb Carthamus tinctorius L, attenuated bleomycin-induced pulmonary fibrosis in mice. This study is to investigate the effect of HSYA on the proliferation and inflammatory level of human fetal lung fibroblasts (MRC-5 cells) induced by tumor necrosis factor-α (TNF-α) and explore the underlying mechanisms. Methods. MRC-5 cells were treated with different concentrations of TNF-α, HSYA, or/and etanercept (ENCP, TNF-α receptor (TNFR1) antagonist, 500 ng/mL) before cell proliferation was detected. The laser confocal microscope was used to observe the role of HSYA in binding of TNF-α and its receptor. Co-immunoprecipitation was used to detect the binding of TNFR1 and TAK1-TAB2 complex. Real-time quantitative RT-PCR and western blot were used to detect the expressions of inflammation-related cytokines and proteins related with the NF-κB pathway. Luciferase reporter gene assay and chromatin coprecipitation method were used to detect the interaction between AP-1 and TGF-β1 promoter. Results. TNF-α (5 ng/mL) was used to induce inflammation and proliferation in MRC-5 cells. HSYA can partially suppress the stimulation of TNF-α on proliferation and inflammatory response of MRC-5 cells. HSYA could compete with TNF-α to bind with TNFR1 and hamper the binding of TNFR1 to TAK1-TAB2 complex. In addition, HSYA could also inhibit the activation of the NF-κB signal pathway and suppress the binding of TGF-β1 promoter with AP-1. Conclusion. Evidence in this study suggested that HSYA affects TNF-α-induced proliferation and inflammatory response of MRC-5 cells through the NF-κB/AP-1 signaling pathway, which may provide theoretical basis for HSYA treatment in pulmonary fibrosis.

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KLF2 attenuates bleomycin-induced pulmonary fibrosis and inflammation with regulation of AP-1

Cited by 23 publications

References 30 publications

Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2)

Montelukast attenuates interleukin IL-1β-induced oxidative stress and apoptosis in chondrocytes by inhibiting CYSLTR1 (Cysteinyl Leukotriene Receptor 1) and activating KLF2 (Kruppel Like Factor 2)

Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction

Hydroxysafflor Yellow A Inhibits TNF-α-Induced Inflammation of Human Fetal Lung Fibroblasts via NF-κB Signaling Pathway

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