MicroRNA-217 modulates inflammation, oxidative stress, and lung injury in septic mice via SIRT1

Yan, Jie; Yang, Fan; Wang, Dengyun; Lü, Yuan; Liu, Li; Wang, Zhengjun

doi:10.1080/10715762.2020.1852234

Cited by 13 publications

(2 citation statements)

References 41 publications

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“…There is growing evidence that miRNAs promote inflammation in ALI by downregulating Sirt1 expression. The downregulation of miR-217 and miR-199a rebounded macrophage Sirt1 levels, and miRNA levels were negatively correlated with Sirt1 levels to achieve anti-inflammatory and antioxidant effects on sepsis-associated ALI in vivo and in vitro, Sirt1 inhibition eliminated the protective effect of miR-217 and miR-199a downregulation on ALI [118,119]. In addition, miR-30d-5p and miR-146a-3p could bind to Sirt1 mRNA 3'-UTR, decrease Sirt1 expression level, and further promote NF-κB inflammatory signaling pathway [120,121].…”

Section: Macrophagesmentioning

confidence: 95%

The Role of Histone Deacetylases in Acute Lung Injury—Friend or Foe

Luo

Liu

et al. 2023

IJMS

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Acute lung injury (ALI), caused by intrapulmonary or extrapulmonary factors such as pneumonia, shock, and sepsis, eventually disrupts the alveolar-capillary barrier, resulting in diffuse pulmonary oedema and microatasis, manifested by refractory hypoxemia, and respiratory distress. Not only is ALI highly lethal, but even if a patient survives, there are also multiple sequelae. Currently, there is no better treatment than supportive care, and we urgently need to find new targets to improve ALI. Histone deacetylases (HDACs) are epigenetically important enzymes that, together with histone acetylases (HATs), regulate the acetylation levels of histones and non-histones. While HDAC inhibitors (HDACis) play a therapeutic role in cancer, inflammatory, and neurodegenerative diseases, there is also a large body of evidence suggesting the potential of HDACs as therapeutic targets in ALI. This review explores the unique mechanisms of HDACs in different cell types of ALI, including macrophages, pulmonary vascular endothelial cells (VECs), alveolar epithelial cells (AECs), and neutrophils.

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Section: Macrophagesmentioning

confidence: 95%

The Role of Histone Deacetylases in Acute Lung Injury—Friend or Foe

Luo

Liu

et al. 2023

IJMS

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“…MicroRNAs (miRNAs) play roles in the posttranscriptional regulation of inflammation 6 – 8 . MiRNAs are a class of endogenous noncoding single-stranded small RNAs-that are 20–24 nucleotides in length.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-146a negatively regulates inflammation via the IRAK1/TRAF6/NF-κB signaling pathway in dry eye

Han

Gao

Wang

et al. 2023

Sci Rep

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Inflammation is a key factor in the pathogenesis of dry eye disease (DED). We aimed to investigate the role of microRNA-146a (miR-146a) in regulating corneal inflammation in a mouse model of benzalkonium chloride (BAC)-induced dry eye and the TNF-α-induced NF-κB signaling pathway in human corneal epithelial cells (HCECs). A mouse model of dry eye was established by administering with BAC to BALB/c mice, and the expression of TNF-α, IL-1β, IL-6, IL-8, cyclooxygenase 2 (COX2), interleukin-1 receptor-associated kinase 1 (IRAK1) and TNF receptor-associated factor 6 (TRAF6) in the corneas of dry eye model mice was significantly increased; this was accompanied by the upregulation of miR-146a and activation of the NF-κB pathway. In vitro, TNF-α induced miR-146a expression in HCECs, while the NF-κB inhibitor SC-514 reduced the expression of miR-146a. Overexpression of miR-146a decreased the expression of IRAK1 and TRAF6, which have been identified as targets of miR-146a. Furthermore, overexpression of miR-146a suppressed NF-κB p65 translocation from the cytoplasm to the nucleus. Moreover, overexpression of miR-146a attenuated the TNF-α-induced expression of IL-6, IL-8, COX2 and intercellular adhesion molecule 1 (ICAM1), while inhibition of miR-146a exerted the opposite effect. Our results suggest that miR-146a mediates the inflammatory response in DED. MiR-146a negatively regulates inflammation in HCECs through the IRAK1/TRAF6/NF-κB pathway, and this may serve as a potential therapeutic approach for the treatment of DED.

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