Hypoxia-Induced HIF-1α Expression Promotes Neurogenic Bladder Fibrosis via EMT and Pyroptosis

Li, Qi; Hong, Yifan; Chen, Jing; Zhou, Xiazhu; Tian, Xiaomao; Yu, Yihang; Shen, Lianju; Chen, Long; Cai, Miao; Wu, Shengde; Wei, Guanghui

doi:10.3390/cells11233836

Cited by 4 publications

(5 citation statements)

References 35 publications

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“…Every rat was a separate experiment unit because of the intervention experiment. Based on the analysis of PASS 15.0 and the primary data collected for our prior study and pre-experiments, whose set power and were 0.85 and 0.05, the sample size was determined [ 14 ]. There were no predetermined inclusion or exclusion criteria that were stated explicitly.…”

Section: Methodsmentioning

confidence: 99%

“…The samples were then divided into sections that were four micrometers thick. Using traditional staining techniques, Masson trichrome and H&E staining were used in the sections to analyze the histomorphology of the rat bladder [ 14 ]. The ImageJ programme (V 1.8.0.112) assessed collagen accumulation (% of total area) in Masson’s stained sections.…”

Section: Methodsmentioning

confidence: 99%

“…The bladder epithelium is one of the main cells responsible for the synthesis of the extracellular matrix [ 13 ]. In our previous study, we discovered that NB rat bladder epithelial cells experience pyroptosis, but whether it plays a role in NB fibrosis is unclear [ 14 ]. As a classic pathway, the downstream inflammatory pathway of NF-κB may be involved in regulating the accumulation of ECM and the cell cycle [ 15 ], and the NOD-like receptor protein 3 (NLRP3) inflammasome is an important component of the inflammatory pathway, which activates Caspase-1 through the NF-κB signaling pathway, causes cellular pyroptosis, and stimulates the maturation and secretion of proinflammatory cytokines (e.g., interleukins, tumor necrosis factor-α) [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of the NF-κB Signaling Pathway Alleviates Pyroptosis in Bladder Epithelial Cells and Neurogenic Bladder Fibrosis

Chen,

Li,

Hong

et al. 2023

IJMS

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Most children with a neurogenic bladder (NB) have bladder fibrosis, which causes irreversible bladder dysfunction and damage to the upper urinary tract. However, the mechanism of bladder fibrosis remains unclear. This study aimed to investigate the underlying causes of bladder fibrosis. Here, the lumbar 6 (L6) and sacral 1 (S1) spinal nerves of Sprague Dawley rats were severed bilaterally to establish NB models. Using RNA-seq, we discovered that the NF-κB signaling pathway and inflammation were upregulated in spinal cord injury (SCI)-induced bladder fibrosis. Subsequent Western blotting, enzyme-linked immunosorbent assays, immunohistochemical staining, and immunofluorescence staining verified the RNA-seq findings. To further clarify whether the NF-κB signaling pathway and pyroptosis were involved in bladder fibrosis, a TGF-β1-treated urinary epithelial cell line (SV-HUC-1 cells) was used as an in vitro model. Based on the results of RNA-seq, we consistently found that the NF-κB signaling pathway and pyroptosis might play important roles in TGF-β1-treated cells. Further experiments also confirmed the RNA-seq findings in vitro. Moreover, using the NLRP3 inhibitor MCC950 rescued TGF-β1-induced fibrosis, and the NF-κB signaling pathway inhibitor BAY 11-7082 effectively rescued TGF-β1-induced pyroptosis and the deposition of extracellular matrix by SV-HUC-1 cells. In summary, our research demonstrated for the first time that the NF-κB signaling pathway inhibition rescued bladder epithelial cells pyroptosis and fibrosis in neurogenic bladders.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inhibition of the NF-κB Signaling Pathway Alleviates Pyroptosis in Bladder Epithelial Cells and Neurogenic Bladder Fibrosis

Chen,

Li,

Hong

et al. 2023

IJMS

Self Cite

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“…Referring to the immunofluorescence experimental procedure described by Li et.al 19 , RAW264.7 cells in different groups were fixed, permeated, blocked, and then incubated with NLRP3 (Cat No. MA5-23919; 1:200) and IL-18 (Cat No IPB0723; 1:200) primary antibodies at 4 °C overnight.…”

Section: Immunofluorescencementioning

confidence: 99%

miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway

Chen,

Zhang,

Huang

et al. 2024

Sci Rep

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Acute lung injury (ALI) is life-threatening. MicroRNAs (miRNAs) are often abnormally expressed in inflammatory diseases and are closely associated with ALI. This study investigates whether miRNA-206-3p attenuates pyroptosis in ALI and elucidates the underlying molecular mechanisms. ALI mouse and cell models were established through lipopolysaccharide (LPS) treatment for 24 h. Subsequently, the models were evaluated based on ultrasonography, the lung tissue wet/dry (W/D) ratio, pathological section assessment, electron microscopy, and western blotting. Pyroptosis in RAW264.7 cells was then assessed via electron microscopy, immunofluorescence, and western blotting. Additionally, the regulatory relationship between miRNA-206-3p and the Toll-like receptor (TLR)4/nuclear factor (NF)-κB/Nod-like receptor protein-3 (NLRP3) pathway was verified. Finally, luciferase reporter gene and RNA pull-down assays were used to verify the targeting relationship between miRNA-206-3p and TLR4. miRNA206-3p levels are significantly decreased in the LPS-induced ALI model. Overexpression of miRNA-206-3p improves ALI, manifested as improved lung ultrasound, improved pathological changes of lung tissue, reduced W/D ratio of lung tissue, release of inflammatory factors in lung tissue, and reduced pyroptosis. Furthermore, overexpression of miRNA-206-3p contributed to reversing the ALI-promoting effect of LPS by hindering TLR4, myeloid differentiation primary response 88 (MyD88), NF-κB, and NLRP3 expression. In fact, miRNA-206-3p binds directly to TLR4. In conclusion, miRNA-206-3p alleviates LPS-induced ALI by inhibiting inflammation and pyroptosis via TLR4/NF-κB/NLRP3 pathway modulation.

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“…Recently, the change in the EMT was observed in the keloid tissues [ 120 ]. Li et al [ 121 ] demonstrated that hypoxia-induced HIF-1α expression significantly promoted neurogenic bladder fibrosis through inducing EMT.…”

Section: The Roles Of Hif-1α In Keloids Formationmentioning

confidence: 99%

Roles of the HIF-1α pathway in the development and progression of keloids

Tai

Zheng

Liao

et al. 2023

Heliyon

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Hypoxia-Induced HIF-1α Expression Promotes Neurogenic Bladder Fibrosis via EMT and Pyroptosis

Cited by 4 publications

References 35 publications

Inhibition of the NF-κB Signaling Pathway Alleviates Pyroptosis in Bladder Epithelial Cells and Neurogenic Bladder Fibrosis

Inhibition of the NF-κB Signaling Pathway Alleviates Pyroptosis in Bladder Epithelial Cells and Neurogenic Bladder Fibrosis

miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway

Roles of the HIF-1α pathway in the development and progression of keloids

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