Pulmonary inflammatory and fibrogenic response induced by graphitized multi-walled carbon nanotube involved in cGAS-STING signaling pathway

Han, Bing; Wang, Xiaoqiao; Wu, Pengfei; Jiang, Huijie; Yang, Qingyue; Li, Siyu; Li, Jiayi; Zhang, Zhigang

doi:10.1016/j.jhazmat.2021.125984

Cited by 51 publications

(27 citation statements)

References 68 publications

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“…Among them, TGF-β1 binds with receptors on the cell membrane and phosphorylating receptor-associated Smad3 proteins, which enhance the expression of α-SMA and Collagen I to promote fibrosis. 23,24 The expressions of TGF-β1 (Fig. 2E and F) and FGF2 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Fucoidans from Cucumaria frondosa ameliorate renal interstitial fibrosis via inhibition of the PI3K/Akt/NF-κB signaling pathway

Song

Zhu

Wu³

et al. 2022

Food Funct.

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Section: Resultsmentioning

confidence: 99%

Fucoidans from Cucumaria frondosa ameliorate renal interstitial fibrosis via inhibition of the PI3K/Akt/NF-κB signaling pathway

Song

Zhu

Wu³

et al. 2022

Food Funct.

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“…In order to extract total RNA from quail cerebrum tissue, Trizol reagent was used. 38,39 RNA concentration was determined by using ultramicro nucleic acid protein analyzer (Implen, N60, Germany), then the RNA was reverse transcribed into cDNA by a cDNA reverse transcription kit (Vazyme, Nanjing). As shown in Table 1, specific primers were synthesized by Sangon Biotech (Shanghai, China).…”

Section: Tunel Assaymentioning

confidence: 99%

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Han

et al. 2022

Environmental Toxicology

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Deltamethrin (DLM) is a widely used and highly effective insecticide. DLM exposure is harmful to animal and human. Quail, as a bird model, has been widely used in the field of toxicology. However, there is little information available in the literature about quail cerebrum damage caused by DLM. Here, we investigated the effect of DLM on quail cerebrum neurons. Four groups of healthy quails were assigned (10 quails in each group), respectively given 0, 15, 30, and 45 mg/kg DLM by gavage for 12 weeks. Through the measurements of quail cerebrum, it was found that DLM exposure induced obvious histological changes, oxidative stress, and neurons apoptosis. To further explore the possible molecular mechanisms, we performed real-time quantitative PCR to detect the expression of endoplasmic reticulum (ER) stressrelated mRNA such as glucose regulated protein 78 kD, activating transcription factor 6, inositol requiring enzyme, and protein kinase RNA (PKR)-like ER kinase. In addition, we detected ATP content in quail cerebrum to evaluate the functional status of mitochondria. The study showed that DLM exposure significantly increased the expression of ER stress-related mRNA and decreased ATP content in quail cerebrum tissues. These results suggest that chronic exposure to DLM induces apoptosis of quail cerebrum neurons via promoting ER stress and mitochondrial dysfunction. Furthermore, our results provide a novel explanation for DLM-induced apoptosis of avian cerebrum neurons.

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“…STING is deeply related to fibrotic disease, including cardiac fibrosis, pulmonary fibrosis, and liver fibrosis ( Luo et al, 2018 ; Li et al, 2022a ; Hu et al, 2022 ). In general, targeting inhibition of STING has an anti-fibrotic effect ( Han et al, 2021 ). Chung K et al reported that STING deficiency or STING inhibitor C-176 ameliorated kidney fibrosis ( Chung et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Inhibition of STING/TBK1 Signaling Attenuates Myeloid Fibroblast Activation and Macrophage to Myofibroblast Transition in Renal Fibrosis

Zeng

Gao

et al. 2022

Front. Pharmacol.

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Renal fibrosis is an important pathological biomarker of chronic kidney disease (CKD). Stimulator of interferon genes/TANK binding kinase 1 (STING/TBK1) axis has been identified as the main regulator of innate immune response and closely related to fibrotic disorder. However, the role of STING/TBK1 signaling pathway in kidney fibrosis is still unknown. In this study, we investigated the effect of pharmacological inhibition of STING/TBK1 signaling on renal fibrosis induced by folic acid (FA). In mice, TBK1 was significantly activated in interstitial cells of FA-injured kidneys, which was markedly inhibited by H-151 (a STING inhibitor) treatment. Specifically, pharmacological inhibition of STING impaired bone marrow-derived fibroblasts activation and macrophage to myofibroblast transition in folic acid nephropathy, leading to reduction of extracellular matrix proteins expression, myofibroblasts formation and development of renal fibrosis. Furthermore, pharmacological inhibition of TBK1 by GSK8612 reduced myeloid myofibroblasts accumulation and impeded macrophage to myofibroblast differentiation, resulting in less deposition of extracellular matrix protein and less severe fibrotic lesion in FA-injured kidneys. In cultured mouse bone marrow-derived monocytes, TGF-β1 activated STING/TBK1 signaling. This was abolished by STING or TBK1 inhibitor administration. In addition, GSK8612 treatment decreased levels of α-smooth muscle actin and extracellular matrix proteins and prevents bone marrow-derived macrophages to myofibroblasts transition in vitro. Collectively, our results revealed that STING/TBK1 signaling has a critical role in bone marrow-derived fibroblast activation, macrophages to myofibroblasts transition, and kidney fibrosis progression.

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Pulmonary inflammatory and fibrogenic response induced by graphitized multi-walled carbon nanotube involved in cGAS-STING signaling pathway

Cited by 51 publications

References 68 publications

Fucoidans from Cucumaria frondosa ameliorate renal interstitial fibrosis via inhibition of the PI3K/Akt/NF-κB signaling pathway

Fucoidans from Cucumaria frondosa ameliorate renal interstitial fibrosis via inhibition of the PI3K/Akt/NF-κB signaling pathway

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Pharmacological Inhibition of STING/TBK1 Signaling Attenuates Myeloid Fibroblast Activation and Macrophage to Myofibroblast Transition in Renal Fibrosis

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