Identification of MicroRNA-92a-3p as an Essential Regulator of Tubular Epithelial Cell Pyroptosis by Targeting Nrf1 via HO-1

Ren-he, Wang; Zhao, Haijun; Zhang, Yingyu; Zhu, Huawei; Su, Qiuju; Qi, Haiyan; Deng, Jun; Xiao, Cheng‐Cheng

doi:10.3389/fgene.2020.616947

Cited by 23 publications

(11 citation statements)

References 40 publications

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“…In addition, it seems that microRNA is also involved in renal I/R injury. Wang et al identified microRNA-92a-3p as an essential regulator of tubular epithelial cell pyroptosis during renal I/R injury by targeting the Nrf1/HO-1 signaling pathway [ 101 ]. Furthermore, unlike aquaporin 4, which is involved in myocardial I/R injury, it is aquaporin 2 that is involved in renal I/R injury.…”

Section: Pyroptosis and I/r Injurymentioning

confidence: 99%

Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury

Zheng

Chi

et al. 2022

Biomolecules

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Ischemia-reperfusion (I/R) injury, uncommon among patients suffering from myocardial infarction, stroke, or acute kidney injury, can result in cell death and organ dysfunction. Previous studies have shown that different types of cell death, including apoptosis, necrosis, and autophagy, can occur during I/R injury. Pyroptosis, which is characterized by cell membrane pore formation, pro-inflammatory cytokine release, and cell burst, and which differentiates itself from apoptosis and necroptosis, has been found to be closely related to I/R injury. Therefore, targeting the signaling pathways and key regulators of pyroptosis may be favorable for the treatment of I/R injury, which is far from adequate at present. This review summarizes the current status of pyroptosis and its connection to I/R in different organs, as well as potential treatment strategies targeting it to combat I/R injury.

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Section: Pyroptosis and I/r Injurymentioning

confidence: 99%

Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury

Zheng

Chi

et al. 2022

Biomolecules

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“…Deng et al found that lncRNA PVT1 could modulate NLRP3-mediated pyroptosis targeting miR-20a-5p in S-AKI [ 31 ]. MicroRNA-92a-3p was identified as an essential regulator of pyroptosis in renal ischemia-reperfusion injury [ 32 ]. The miR-223-3p/NLRP3 pathway is involved in the LPS-induced AKI and inhibits HK-2 cell pyroptosis [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

miR-181a-5p Inhibits Pyroptosis in Sepsis-Induced Acute Kidney Injury through Downregulation of NEK7

Zhang

Zhi

Lin

et al. 2022

Journal of Immunology Research

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Sepsis is a life-threatening organ dysfunction caused by the uncontrolled inflammation, easily affecting the kidney. Sepsis-induced acute kidney injury (S-AKI) has high morbidity and mortality, of which the pathophysiological mechanisms have not been completely illuminated, leading to nonspecific therapies. Specific microRNAs were related with the pathogenesis of AKI. However, only limited studies focused on the pyroptosis in the context of S-AKI. The in vitro LPS-induced HK-2 cell model and in vivo CLP-induced mouse model were established. qRT-PCR, Western blot, ELISA, and RNA pulldown were used for expression examination. Multiple biological databases were used for miRNA screening. H&E staining and IHC staining were performed. The LPS-induced HK-2 cells showed significantly increased ( P < 0.01 ) fluorescence intensity of N-GSDMD and ASC compared with the HK-2 cells. The expression of NLRP3, NEK7, ASC, active caspase-1, and N-GSDMD was significantly enhanced ( P < 0.05 ) and the inflammatory factors including IL-18, IL-1β, and THF-α were all increased in LPS-induced HK-2 cells and CLP-induced mice. Renal edema, serum Cr and BUN, and expression of KIM-1 and NGAL were significantly higher ( P < 0.05 ) in CLP-induced S-AKI mice than the sham group. miR-101-3p, miR-144-3p, miR-181a-5p, miR-4262, and miR-513b-5p could inhibit NEK7. NEK7 is an interacting protein of miRNA-181a-5p. miR-181a-5p inhibits pyroptosis of the LPS-induced HK-2 cells through downregulation of NEK7. Pyroptosis of HK-2 cells promotes inflammation. miR-181a-5p inhibits pyroptosis through downregulation of NEK7 in LPS-induced HK-2 cells and CLP-induced mice. Our study indicated miR-181a-5p as a new potential therapeutic target for S-AKI therapy.

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“…the therapeutic mechanism of PUFA ω-3, we measured the NRF1/HMOX1 protein expression, a classical pathway associated with oxidative stress [27,28]. PUFA ω-3 upregulated Nrf1 and Hmox1 expression when compared with that in the model group (Fig 4F and 4G).…”

Section: Plos Onementioning

confidence: 99%

Supplementation with dietary omega-3 PUFA mitigates fetal brain inflammation and mitochondrial damage caused by high doses of sodium nitrite in maternal rats

Sun

Zhang

2022

PLoS ONE

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Objective Food safety and nutrition during pregnancy are important concerns related to fetal brain development. In the present study, we aimed to explore the effects of omega-3 polyunsaturated fatty acids (PUFA ω-3) on exogenous sodium nitrite intervention-induced fetal brain injury in pregnant rats. Methods During pregnancy, rats were exposed to water containing sodium nitrite (0.05%, 0.15%, and 0.25%) to establish a fetal rat brain injury model. Inflammatory factors and oxidative stress levels were detected using enzyme-linked immunosorbent assay (ELISA) or flow cytometry. Subsequently, animals were divided into three groups: control, model, and 4% PUFA ω-3. Pregnancy outcomes were measured and recorded. Hematoxylin-eosin (H&E) staining and immunohistochemistry (IHC) were utilized to observe brain injury. ELISA, quantitative real-time PCR (qRT-PCR), western blot, flow cytometry, and transmission electron microscopy (TEM) were adopted to measure the levels of inflammatory factors, the NRF1/HMOX1 signaling pathway, and mitochondrial and oxidative stress damage. Results With the increase of sodium nitrite concentration, the inflammatory factors and oxidative stress levels increased. Therefore, the high dose group was set as the model group for the following experiments. After PUFA ω-3 treatment, the fetal survival ratio, average body weight, and brain weight were elevated. The cells in the PUFA ω-3 group were more closely arranged and more round than the model. PUFA ω-3 treatment relieved inflammatory factors, oxidative stress levels, and mitochondria damage while increasing the indicators related to brain injury and NRF1/HMOX1 levels. Conclusions Sodium nitrite exposure during pregnancy could cause brain damage in fetal rats. PUFA ω-3 might help alleviate brain inflammation, oxidative stress, and mitochondrial damage, possibly through the NRF1/HMOX1 signaling pathway. In conclusion, appropriately reducing sodium nitrite exposure and increasing PUFA omega-3 intake during pregnancy may benefit fetal brain development. These findings could further our understanding of nutrition and health during pregnancy.

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Identification of MicroRNA-92a-3p as an Essential Regulator of Tubular Epithelial Cell Pyroptosis by Targeting Nrf1 via HO-1

Cited by 23 publications

References 40 publications

Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury

Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury

miR-181a-5p Inhibits Pyroptosis in Sepsis-Induced Acute Kidney Injury through Downregulation of NEK7

Supplementation with dietary omega-3 PUFA mitigates fetal brain inflammation and mitochondrial damage caused by high doses of sodium nitrite in maternal rats

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