FoxF1 protects rats from paraquat-evoked lung injury following HDAC2 inhibition via the microRNA-342/KLF5/IκB/NF-κB p65 axis

Zheng, Fenshuang; Liu, Tao; Zhu, Junbo; Xie, Yuan; Wu, Lianjun; Lin, Zhaoheng

doi:10.1016/j.yexcr.2020.112208

Cited by 11 publications

(5 citation statements)

References 22 publications

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“…Various types of medical treatments are available for childhood asthma; however, their efficacy remains unsatisfactory (19)(20)(21). In the present study, a mechanism of action of asthma was examined that demonstrated FOXF1 may FOXF1 plays an important role in regulating lung development and lung injury (22). A previous study has shown that FOXF1 stimulates pulmonary angiogenesis and alveolation during recovery from neonatal hyperoxia injury (23).…”

Section: Discussionmentioning

confidence: 86%

“…FOXF1 plays an important role in regulating lung development and lung injury ( 22 ). A previous study has shown that FOXF1 stimulates pulmonary angiogenesis and alveolation during recovery from neonatal hyperoxia injury ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, FOXF1 maintains endothelial barrier function and prevents edema following lung injury ( 15 ). A previous study has shown that FOXF1 protects against BEAS-2B apoptosis and oxidative stress induced by paraquat ( 22 ). Therefore, it is speculated that FOXF1 is involved in the regulation of airway epithelial cell injury induced by asthma.…”

Section: Discussionmentioning

confidence: 99%

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FOXF1 attenuates TGF‑β1‑induced bronchial epithelial cell injury by inhibiting CDH11‑mediated Wnt/β‑catenin signaling

Chen

Liu

et al. 2023

Exp Ther Med

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Forkhead box F1 (FOXF1) has been reported to be associated with lung development. However, the role of FOXF1 in asthma is still not fully understood. In the present study, the biological role and the potential mechanism of FOXF1 was explored in transforming growth factor β1 (TGF-β1)-induced bronchial epithelial cell injury. Reverse transcription-quantitative PCR and western blotting were performed to detect the expression levels of FOXF1 and cadherin (CDH) 11 in TGF-β1-induced bronchial epithelial cells. Proliferation, apoptosis and inflammation were assessed using Cell Counting Kit-8 assay, f low cytometry, western blotting and ELISA. Fibrosis and epithelial-mesenchymal transition (EMT) were evaluated using immunofluorescence and western blotting. The expression levels of the proteins involved in the Wnt/β-catenin pathway were detected by western blotting. The results indicated that FOXF1 expression was downregulated, while CDH11 expression was upregulated in TGF-β1-treated BEAS-2B cells. FOXF1 overexpression promoted proliferation, inhibited induction of apoptosis and suppressed the inflammatory response of BEAS-2B cells exposed to TGF-β1. In addition, FOXF1 overexpression restrained TGF-β1-induced bronchial epithelial fibrosis and EMT and inhibited the activation of the Wnt/β-catenin pathway. CDH11 overexpression reversed the effects of FOXF1 overexpression on proliferation, apoptosis, fibrosis, EMT and inflammation by regulating the Wnt/β-catenin pathway. Collectively, the results of the present study suggested that FOXF1 regulated TGF-β1-induced BEAS-2B cell injury by inhibiting CDH11-mediated Wnt/β-catenin signaling. This may provide a novel therapeutic strategy for the treatment of asthma.

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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FOXF1 attenuates TGF‑β1‑induced bronchial epithelial cell injury by inhibiting CDH11‑mediated Wnt/β‑catenin signaling

Chen

Liu

et al. 2023

Exp Ther Med

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“… 37 , 51 , 53 In a study on lung injury, miR-342 inhibited oxidative stress in human bronchial epithelial cells by targeting KLF5, suggesting inhibition of oxidative stress may also be the mechanism by which miR-342-5p exerts its neuroprotective effect in AIS. 54 In our study, we discovered that attenuated oxidative stress and ameliorated neurological deficits were a reflection of increased miR-342-5p. This positive effect of miR-342-5p on AIS is consistent with the earlier findings.…”

Section: Discussionmentioning

confidence: 67%

Circ_0008146 Exacerbates Ferroptosis via Regulating the miR-342-5p/ACSL4 Axis After Cerebral Ischemic/Reperfusion

Liu,

Peng,

Wang

et al. 2024

JIR

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Purpose Acute ischemic stroke (AIS) has seriously threatened people’s health worldwide and there is an urge need for early diagnosis and effective treatment of AIS. This research intended to clarify the regulatory role of circ_0008146/miR-342-5p/ACSL4 axis in AIS. Methods High-throughput small RNA sequencing analysis was adapted to identify differentially expressed miRNAs between the AIS and control group. The circ_0008146, miR-342-5p, and ACSL4 levels were detected by qRT-PCR. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. Assay kits were used to determine Fe 2+ levels and a battery of oxidative stress and lipid peroxidation indicators, including ROS, MDA, LPO, SOD and GSH/GSSG ratio. The protein levels of ACSL4 were measured by Western blot. The behavioral function was assessed using neurobehavioral tests. TTC staining was employed to visualize infarction size. Nissl staining was adapted to detect histopathological changes. Receiver operating characteristic curve and correlation analysis were applied to investigate the clinical value and association of miR-342-5p and ACSL4. Results A total of 44 AIS patients and 49 healthy controls were enrolled in our study. The small RNA sequencing unveiled a significant decrease in miR-342-5p levels in AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic/reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. Circ_0008146 acted as a sponge of miR-342-5p, and overexpression of circ_0008146 increased neurological deficits and brain injury in mice. Circ_0008146 contributed to ferroptosis in cerebral infarction via sponging miR-342-5p to regulate ACSL4. Plasma miR-342-5p and ACSL4 demonstrated significant correlation and good diagnostic value for AIS patients. Conclusion This study provides the first in vivo evidence to show that circ_0008146 exacerbates neuronal ferroptosis after AIS via the miR-342-5p/ACSL4 axis. Furthermore, miR-342-5p/ACSL4 axis holds promise as a viable therapeutic target and practical biomarkers for AIS patients.

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“…In addition, CYP4B1 may hold significance in the prognosis of lung adenocarcinoma [ 29 ] and the progression of urothelial carcinoma [ 30 ]. Foxf1 is related to lung development [ 31 ], and extensive research has been conducted on this gene. FOXF1 has been confirmed to affect pulmonary angiogenesis in alveolar capillary dysplasia [ 32 – 34 ].…”

Section: Discussionmentioning

confidence: 99%

Investigation into the role of H2-Ab1 in vascular remodeling in pulmonary arterial hypertension via Bioinformatics

Wang,

Wang

2024

BMC Pulm Med

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Background Pulmonary arterial hypertension (PAH) is a progressive disease of vascular remodeling characterized by persistent pulmonary arterial pressure elevation, which can lead to right heart failure and premature death. Given the complex pathogenesis and poor prognosis of PAH, the identification and investigation of biomarkers become increasingly critical for advancing further understanding of the disease. Methods PAH-related datasets, GSE49114, GSE180169 and GSE154959, were downloaded from the publicly available GEO database. By performing WGCNA on the GSE49114 dataset, a total of 906 PAH-related key module genes were screened out. By carrying out differential analysis on the GSE180169 dataset, a total of 576 differentially expressed genes were identified. Additionally, the GSE154959 single-cell sequencing dataset was also subjected to differential analysis, leading to the identification of 34 DEGs within endothelial cells. By taking intersection of the above three groups of DEGs, five PAH-related hub genes were screened out, namely Plvap, Cyp4b1, Foxf1, H2-Ab1, and H2-Eb1, among which H2-Ab1 was selected for subsequent experiments. Results A SuHx mouse model was prepared using the SU5416/hypoxia method, and the successful construction of the model was evaluated through Hematoxylin-Eosin staining, hemodynamic detection, fulton index, and Western Blot (WB). The results of WB and qRT-PCR demonstrated a significant upregulation of H2-Ab1 expression in SuHx mice. Consistent with the results of bioinformatics analysis, a time-dependent increase was observed in H2-Ab1 expression in hypoxia-treated mouse pulmonary artery endothelial cells (PAECs). To investigate whether H2-Ab1 affects the development and progression of PAH, we knocked down H2-Ab1 expression in PAECs, and found that its knockdown inhibited the viability, adhesion, migration, and angiogenesis, while concurrently promoted the apoptosis of PAECs. Conclusion H2-Ab1 could regulate the proliferation, apoptosis, adhesion, migration, and angiogenesis of PAECs.

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FoxF1 protects rats from paraquat-evoked lung injury following HDAC2 inhibition via the microRNA-342/KLF5/IκB/NF-κB p65 axis

Cited by 11 publications

References 22 publications

FOXF1 attenuates TGF‑β1‑induced bronchial epithelial cell injury by inhibiting CDH11‑mediated Wnt/β‑catenin signaling

FOXF1 attenuates TGF‑β1‑induced bronchial epithelial cell injury by inhibiting CDH11‑mediated Wnt/β‑catenin signaling

Circ_0008146 Exacerbates Ferroptosis via Regulating the miR-342-5p/ACSL4 Axis After Cerebral Ischemic/Reperfusion

Investigation into the role of H2-Ab1 in vascular remodeling in pulmonary arterial hypertension via Bioinformatics

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