Macrophage micro-RNA-155 promotes lipopolysaccharide-induced acute lung injury in mice and rats

Wang, Wen; Li, Zhi; Su, Jie; Chen, Wensheng; Wang, Xiaowu; Bai, San-Xing; Zhang, Jinzhou; Yu, Shiqiang

doi:10.1152/ajplung.00001.2016

Cited by 58 publications

(54 citation statements)

References 52 publications

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“…Its severity was increased as dose increases and time goes which was consistent with our previous studies [14]. The study have shown that miR-155 downregulated SOCS-1 expression by binding to the 3'-UTR of the SOCS-1 mRNA , and it can promote the inflammatory response during lung injury as a proinflammatory factor [20]. Previous study has indicated that miR-155 may enhance inflammatory response by stimulating the release of inflammatory mediators by targeting several negative feedback molecules, including SH2 domaincontaining inositol 5'-phosphatase (SHIP)-1 [21].…”

Section: The Expression Of Microrna-155 and 127 In The Neonatal Sd Rasupporting

confidence: 91%

The expression of microRNA-155 and 127 in the neonatal SD rats with acute lung injury induced by lipopolysaccharide

Liu¹,

Li²,

Hu³

et al. 2018

biomedicalresearch

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Aim: This study was to observe the changes of the gene expression of microRNA-155 and 127 in the neonatal rats with Acute Lung Injury (ALI). Methods: Eighty neonatal SD rats were randomly divided into experimental groups (intraperitoneal injection with LPS, n=60) and control (intraperitoneal injection with NS, n=20). Neonatal rats in experimental groups (LPS 1 mg, 2 mg and 3 mg group, n=20) were received corresponding dose of LPS (1, 2 and 3 mg/kg, diluted with saline to 0.2 ml), while neonatal rats in control group were injected 0.2 ml saline respectively. Then we killed rats at 1 h, 6 h, 12 h and 24 h respectively in each group. The lung general pathological changes were observed. The expression of microRNA-155 and 127 were detected by semi-quantitative reverse transcription-polymerase chain reaction. Tumor Necrosis Factor-α (TNF-α) and Interleukelin-6 (IL-6) in Bronchoalveolar Lavage Fluid (BALF) were detected by enzyme-linked immunosorbent assay. The expression of TNF-α and IL-6 protein in lung tissue were detected by western blotting. Results: The expression of microRNA-155 was up-regulated in the tissues and BALF in a dose and timedependent manner and microRNA-127 down-regulated. The difference were statistically significant when compared with the control group (all P<0.05). The TNF-α and IL-6 level of BALF rats with ALI in LPS groups were increased compared with the control group in a dose-dependent manner (all P<0.05). A similar trend had been seen in TNF-α and IL-6 protein level of lung tissues, the difference was statistically significant. Conclusion: The expression of microRNA-155 and 127 are associated with severity of the ALI in a dose and time-dependent manner, and they might be considered as potential biomarkers for early diagnosis of ALI.

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Section: The Expression Of Microrna-155 and 127 In The Neonatal Sd Rasupporting

confidence: 91%

The expression of microRNA-155 and 127 in the neonatal SD rats with acute lung injury induced by lipopolysaccharide

Liu¹,

Li²,

Hu³

et al. 2018

biomedicalresearch

View full text Add to dashboard Cite

show abstract

“…Among these factors, microRNA (miRNAs) are critical regulators, with the capacity to target multiple messenger RNAs involved in the EndoMT process and disease progression regulation . MiR‐155 is a key mediator in the process of pulmonary fibrosis, besides in other lung diseases as allergic airway inflammation, lung injury, and lung cancer . However, opposing effects of miR‐155, anti‐fibrotic or fibrotic, in experimental and idiopathic pulmonary fibrosis have been reported .…”

Section: Discussionmentioning

confidence: 99%

SHIP‐1, a target of miR‐155, regulates endothelial cell responses in lung fibrosis

Tang

Mao

et al. 2019

FASEB j.

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Src Homology 2‐containing Inositol Phosphatase‐1 (SHIP‐1) is a target of miR‐155, a pro‐inflammatory factor. Deletion of the SHIP‐1 gene in mice caused spontaneous lung inflammation and fibrosis. However, the role and function of endothelial miR‐155 and SHIP‐1 in lung fibrosis remain unknown. Using whole‐body miR‐155 knockout mice and endothelial cell–specific conditional miR‐155 (VEC‐Cre‐miR‐155 or VEC‐miR‐155) or SHIP‐1 (VEC‐SHIP‐1) knockout mice, we assessed endothelial‐mesenchymal transition (EndoMT) and fibrotic responses in bleomycin (BLM) induced lung fibrosis models. Primary mouse lung endothelial cells (MLEC) and human umbilical vein endothelial cells (HUVEC) with SHIP‐1 knockdown were analyzed in TGF‐β1 or BLM, respectively, induced fibrotic responses. Fibrosis and EndoMT were significantly reduced in miR‐155KO mice and changes in EndoMT markers in MLEC after TGF‐β1 stimulation confirmed the in vivo findings. Furthermore, lung fibrosis and EndoMT responses were reduced in VEC‐miR‐155 mice but significantly enhanced in VEC‐SHIP‐1 mice after BLM challenge. SHIP‐1 knockdown in HUVEC cells resulted in enhanced EndoMT induced by BLM. Meanwhile, these changes involved the PI3K/AKT, JAK/STAT3, and SMAD/STAT signaling pathways. These studies demonstrate that endothelial miR‐155 plays an important role in fibrotic responses in the lung through EndoMT. Endothelial SHIP‐1 is essential in controlling fibrotic responses and SHIP‐1 is a target of miR‐155. Endothelial cells are an integral part in lung fibrosis.

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“…A final element of the study that affects interpretation of the results is the use of the cellular fraction of blood to study peripheral cytokine expression (Wang et al, 2016; Opstad et al, 2017). Although it is more common in contemporary studies to utilize plasma protein measures to detect cytokines, cytokines in plasma have very short half-lives and the assays to measure them require comparatively large samples.…”

Section: Discussionmentioning

confidence: 99%

Adolescent Ethanol Exposure Leads to Stimulus-Specific Changes in Cytokine Reactivity and Hypothalamic-Pituitary-Adrenal Axis Sensitivity in Adulthood

Vore

Doremus-Fitzwater

Gano

et al. 2017

Front. Behav. Neurosci.

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Adolescent alcohol use comprises a significant public health concern and is often characterized by binge-like consumption patterns. While ethanol exposure in adulthood has been shown to alter the stress response, including the Hypothalamic–Pituitary–Adrenal (HPA) axis, few studies have examined whether binge-like ethanol exposure during adolescence results in enduring changes in HPA axis sensitivity in adulthood. In the present studies, adolescent Sprague-Dawley rats were given intragastric (i.g.) intubations of ethanol (4 g/kg) or vehicle once per day for three consecutive days, beginning on postnatal day (P) 30 (±1). This exposure was followed by a 2-day period of rest/withdrawal. Rats received a total of either two (Experiments 1, 2 and 3) or four (Experiment 4) cycles of ethanol exposure and were subsequently allowed to age normally until adulthood. In Experiment 1, adult, (P71–75), ethanol- or vehicle-exposed rats received a 60 min restraint stress challenge. In Experiment 2, rats received a 50 μg/kg injection of lipopolysaccharide (LPS). In Experiment 3, rats received a challenge of 2.5 g/kg ethanol (intraperitoneally; i.p.). In Experiment 4, male and female ethanol- or vehicle- exposed rats received a 50 μg/kg injection of LPS. In all experiments, blood samples were collected for later assessment of corticosterone (CORT), blood ethanol concentrations (BECs), and the cellular fraction of blood was analyzed for cytokine gene expression. As expected, all three challenges led to a time-dependent surge in CORT. Gene expression analyses of cytokines (Interleukin [IL]-6, IL-1β, and Tumor necrosis factor alpha [TNFα]) from the cellular fraction of blood revealed unique, time-dependent patterns of cytokine expression depending upon the nature of the adult challenge incurred (restraint, LPS, or EtOH). Importantly, adolescent ethanol exposure led to attenuated restraint and LPS-induced cytokine expression in males, whereas female rats displayed an absence of cytokine alterations, and a tendency toward heightened HPA axis reactivity. These findings suggest that adolescent ethanol exposure may cause lasting alterations in cytokine regulation and HPA axis sensitivity that (a) persist into adulthood; (b) may vary depending on the nature of the challenge incurred during adulthood; and that (c) are sex-specific.

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Macrophage micro-RNA-155 promotes lipopolysaccharide-induced acute lung injury in mice and rats

Cited by 58 publications

References 52 publications

The expression of microRNA-155 and 127 in the neonatal SD rats with acute lung injury induced by lipopolysaccharide

The expression of microRNA-155 and 127 in the neonatal SD rats with acute lung injury induced by lipopolysaccharide

SHIP‐1, a target of miR‐155, regulates endothelial cell responses in lung fibrosis

Adolescent Ethanol Exposure Leads to Stimulus-Specific Changes in Cytokine Reactivity and Hypothalamic-Pituitary-Adrenal Axis Sensitivity in Adulthood

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