Correlations of inflammation, oxidative stress and prognosis with expression of lncRNA H19 in rats with sepsis-evoked lung injury

Cui, Changxing; Chen, Xiaoxue; Du, Wenjie; Jing, Lihong; Shi, Lei; Xia, Di; Jiang, Tao

doi:10.23736/s0031-0808.19.03851-5

Cited by 3 publications

(3 citation statements)

References 4 publications

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“…Growing evidence indicates that lncRNAs are key modulators of various physiological and pathological processes in disease states, including cell proliferation, invasion, migration, and apoptosis [ 14 , 15 ]. In recent years, studies have shown that lncRNA CASC9 [ 16 ], TUG1 [ 17 ], H19 [ 18 ], and MALAT1 [ 19 ] are associated with sepsis-induced lung injury and pulmonary inflammatory response. However, it is unknown about ASLNC12002 in regulating pulmonary fibrosis during sepsis-derived ARDS.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA-ASLNC12002 alleviates epithelial–mesenchymal transition of type II alveolar epithelial cells in sepsis-induced acute respiratory distress syndrome

et al. 2022

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Patients with sepsis-induced acute respiratory distress syndrome (ARDS) have higher mortality and poor prognosis than pneumonia-induced ARDS. Pulmonary fibrosis is an irreversible accumulation of connective tissue in the interstitium of the lung and closely associated with the epithelial–mesenchymal transition (EMT) of type II alveolar epithelial cells (AECIIs). Therefore, it is undoubtedly worth studying whether the EMT of AECIIs in sepsis-induced ARDS patients is different from that in patients with pneumonia-induced ARDS in the regulatory mechanism. Here, we will report for the first time that an lncRNA-ASLNC12002 is highly expressed in AECIIs of patients with sepsis-induced pneumonia and promotes EMT in AECIIs. The research results showed that the expression of ASLNC12002 in AECIIs derived from patients with sepsis-induced ARDS is significantly higher than that in normal people and pneumonia-induced ARDS patients. Mechanism research showed that ASLNC12002 can cause the inactivation of the anti-EMT pathway NR2F2/miR128-3p/Snail1 by acting as the sponge of miR128-3p. Functional experiments showed that targeted silencing of ASLNC12002 could effectively inhibit EMT progression in AECIIs of patients with sepsis-induced pneumonia by restoring NR2F2/miR128-3p/Snail1 pathway. In a word, our study shows for the first time that the inactivation of NR2F2/miR128-3p/Snail1 pathway caused by the enhanced expression of ASLNC12002 is the direct reason why AECIIs in sepsis-induced ARDS patients are prone to get EMT progress. ASLNC12002 has the potential to become a biological target for the prevention and treatment of pulmonary fibrosis in patients with sepsis-induced ARDS. At the same time, the expectation that ASLNC12002 and its related products may be used as clinical markers for the evaluation of early pulmonary fibrosis in ARDS patients should not be ignored.

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Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA-ASLNC12002 alleviates epithelial–mesenchymal transition of type II alveolar epithelial cells in sepsis-induced acute respiratory distress syndrome

et al. 2022

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“…Recent evidence suggests that H19 plays a regulatory role in mouse pulmonary microvascular endothelial cells (PMVECs) [20]. Meanwhile, H19 is recognized as an inhibitory factor of sepsis-induced kidney injury and ALI [21,22]. It has previously been observed that H19 is downregulated in mice with LPS-induced sepsis [23] and in sera of sepsis patients [24].…”

Section: Introductionmentioning

confidence: 99%

“…It has previously been observed that H19 is downregulated in mice with LPS-induced sepsis [23] and in sera of sepsis patients [24]. Additionally, existing research recognizes the correlation between H19 and inflammatory reaction and oxidative stress in rats with sepsis-triggered ALI [22]. However, the previous studies of lncRNA H19 have not dealt with the action and concrete mechanism of H19 in sepsis-evoked ALI.…”

Section: Introductionmentioning

confidence: 99%

LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis

Hao

Wei

2022

BMC Pulm Med

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Objective Acute lung injury (ALI) increases sepsis morbidity and mortality. LncRNA H19 plays a critical role in sepsis. miR-107 is highly-expressed and TGFβ type III receptor (TGFBR3) is poorly-expressed in sepsis, yet their roles in sepsis development require further investigation. This study aimed to investigate the mechanism of H19 in alleviating sepsis-induced ALI through the miR-107/TGFBR3 axis. Methods Mice were intravenously injected with Ad-H19 adenovirus vector or control vector one week before establishing the mouse model of cecal ligation and puncture (CLP). Pulmonary microvascular endothelial cells (PMVECs) were transfected with oe-H19 or oe-NC plasmids and then stimulated by lipopolysaccharide (LPS). Lung injury was assessed via hematoxylin–eosin staining, measurement of wet-to-dry (W/D) ratio, and TUNEL staining. Levels of H19, miR-107, and TGFBR3 were determined by RT-qPCR. Apoptosis of PMVECs was evaluated by flow cytometry. Levels of Bax and Bcl-2 in lung tissues and PMVECs were measured using Western blot. Total protein concentration and the number of total cells, neutrophils, and macrophages in bronchoalveolar lavage fluid (BALF) were quantified. Levels of TNF-α, IL-1β, IL-6, and IL-10 in BALF, lung tissues, and PMVECs were measured by ELISA. Cross-linking relationships among H19, miR-107 and TGFBR3 were verified by dual-luciferase and RIP assays. Results H19 was poorly-expressed in CLP-operated mice. H19 overexpression attenuated sepsis-induced ALI, which was manifested with complete alveolar structure, decreased lung injury score and lung W/D ratio, and inhibited apoptosis in CLP-operated mice, which was manifested with decreased number of TUNEL-positive cells and Bax level and increased Bcl-2 level. CLP-operated mice had increased concentration of total protein and number of total cells, neutrophils, and macrophages in BALF, which was nullified by H19 overexpression. H19 overexpression declined levels of TNF-α, IL-1β, and IL-6 and elevated IL-10 levels. H19 inhibited LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production. H19 targeted TGFBR3 as the ceRNA of miR-107. miR-107 overexpression or silencing TGFBR3 partially averted the inhibition of H19 overexpression on LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production. Conclusion LncRNA H19 inhibited LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production and attenuated sepsis-induced ALI by targeting TGFBR3 as the ceRNA of miR-107.

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LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis

Shu

Liu

et al. 2020

Inflammation

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Correlations of inflammation, oxidative stress and prognosis with expression of lncRNA H19 in rats with sepsis-evoked lung injury

Cited by 3 publications

References 4 publications

Knockdown of lncRNA-ASLNC12002 alleviates epithelial–mesenchymal transition of type II alveolar epithelial cells in sepsis-induced acute respiratory distress syndrome

Knockdown of lncRNA-ASLNC12002 alleviates epithelial–mesenchymal transition of type II alveolar epithelial cells in sepsis-induced acute respiratory distress syndrome

LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis

LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis

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