MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

Zhang, Yue; Xie, Yifang; Zhang, Leifang; Zhao, Hang

doi:10.3390/molecules25051022

Cited by 15 publications

(7 citation statements)

References 44 publications

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“… 71 Also, smoking can cause impairment in miR-155 expression that induces acute lung injury by targeting SOCS1 and emphysema. 72 , 73 In our, study we did not find a significant association between smoking and miR-155 expression. On the contrary, we found a significant increase in STAT3/JAK2 expression and smoking.…”

Section: Discussioncontrasting

confidence: 67%

Circulating miR-155 and JAK2/STAT3 Axis in Acute Ischemic Stroke Patients and Its Relation to Post-Ischemic Inflammation and Associated Ischemic Stroke Risk Factors

Sadik¹,

Rashed²,

Mawla³

2021

IJGM

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Background “Micro RNAs and their target genes recently have been identified to play a crucial role in the molecular pathogenesis of post-stroke ischemic cellular injury, which elucidates their new role in ischemic stroke diagnosis and therapy”. Thus, we evaluated the relative serum expression of miR-155, an inflammatory micro RNA, and the mRNAs (JAK2/STAT3) in acute ischemic stroke patients and its associations with the inflammatory cytokine TNF-α and different stroke risk factors. Subjects and Methods The relative expression of serum miR-155 and mRNAs (JAK2/STAT3) was assessed using RT-PCR, serum TNF-α was measured using ELIZA in 46 acute ischemic stroke patients and 50 control subjects. Receiver operating characteristic (ROC) curve was constructed to assess the specificity and sensitivity of circulating miR-155, JAK2/STAT3 as biomarkers for acute ischemic stroke. Results Circulating miR-155, JAK2/STAT3 were significantly up-regulated among stroke patients (8.5, 2.9, 4.2 fold respectively, P <0.001) with significant increase in TNF-α (263.8 ± 10.7 pg/mL, P <0.001). MiR-155, JAK2/STAT3 were positively correlated with TNF-α. MiR-155, JAK2/STAT3 were significantly increased in stroke patients and associated with risk factors such as hypertension, carotid atherosclerosis, and atrial fibrillation. Our study revealed that miR-155 has diagnostic accuracy for acute ischemic stroke where AUC=0.9, ( P <0.001). Conclusion The elevated expressions of circulating miR-155, JAK2/STAT3, and TNF-α in acute ischemic stroke patients could trigger post-stroke cellular inflammation. MiR-155 could be used as potential inflammatory biomarker for acute ischemic stroke. However, further clinical studies are still needed to determine the exact role of miRNAs and different signal transduction expressions in the stage of acute ischemic stroke.

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Section: Discussioncontrasting

confidence: 67%

Circulating miR-155 and JAK2/STAT3 Axis in Acute Ischemic Stroke Patients and Its Relation to Post-Ischemic Inflammation and Associated Ischemic Stroke Risk Factors

Sadik¹,

Rashed²,

Mawla³

2021

IJGM

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“…Moreover, Li et al revealed that MALAT1 alleviated the ox-low density lipoproteins (ox-LDL)-induced inflammation and apoptosis of Human Coronary Artery Endothelial Cells (HCAECs) via sponging miR-155 to increase the SOCS-1 level [43]. In our previous study, we also proved the relationships of miR-155 and SOCS-1 in smoke-induced ALI mice [44]. Thus, it is worth exploring the underlying mechanism.…”

Section: Discussionmentioning

confidence: 52%

LncRNA MALAT1 Participates in Protection of High-Molecular-Weight Hyaluronan against Smoke-Induced Acute Lung Injury by Upregulation of SOCS-1

Lang

et al. 2022

Molecules

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Smoke-induced acute lung injury (ALI) is a grievous disease with high mortality. Despite advances in medical intervention, no drug has yet been approved by the Food and Drug Administration (FDA) for ALI. In this study, we reported that pretreatment with high-molecular-weight hyaluronan (1600 kDa, HA1600) alleviated pulmonary inflammation and injury in mice exposed to smoke and also upregulated long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), as well as suppressor of cytokine signaling-1 (SOCS-1), in the lung tissues. Next, we overexpressed MALAT1 in the lungs by intratracheal administration of adenovirus cloned with MALAT1 cDNA and found that the survival of mice after smoke exposure was improved. Moreover, pulmonary overexpression of MALAT1 ameliorated smoke-induced ALI in mice and elevated the level of SOCS-1 in the lungs. In conclusion, the results pointed out that HA1600 exerted a protective effect against smoke-induced ALI through increasing the MALAT1 level and the subsequent SOCS-1 expression. Our study provides a potential therapeutic approach to smoke-induced ALI and a novel insight into the mechanism of action of HA1600.

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“…For example, Song et al (2021) demonstrated that the core miRNA biogenesis and targeting machinery were essential for the IFNγ-activated JAK-STAT signaling and antigen presentation in cancer cells, largely by controlling miR-155-targeted silencing of SOCS-1 . In smoke inhalation-induced lung injury, miRNA-155 was involved in the inflammatory response by inhibiting the expression of SOCS-1 ( Zhang et al, 2020 ). Wang et al (2018) also illustrated that HBeAg augmented the expression of miR-155 to promote inflammatory cytokine production by inhibiting the expression of SOCS-1.…”

Section: Discussionmentioning

confidence: 99%

CpG Island Methylation of Suppressor of Cytokine Signaling-1 Gene Induced by HCV Is Associated With HCV-Related Hepatocellular Carcinoma

Liu

Xing

et al. 2022

Front. Microbiol.

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Suppressor of cytokine signaling 1 (SOCS-1) is implicated in both virus infection and carcinogenesis. This study investigated the role of HCV infection on SOCS-1 in normal and HCV-infected tissues and revealed a possible mechanism underlying HCV-induced hepatocellular carcinoma (HCC) genesis. In total, 10 HCV-HCC tissues, seven adjacent tissues, seven distal tissues, and 16 normal liver tissues were collected. SOCS-1 expression in tissue sections was detected by immunohistochemistry. After viral load was quantified, the correlation between SOCS-1 expression and viral load was analyzed in different tissues. Then, HCV replicon model was used to detect a relationship between HCV and SOCS-1. Subsequently, methylation-specific PCR (MSP) was applied to show the methylation status of SOCS-1 genes in normal tissues and HCV-replicating cell lines. A correlation between gene methylation, SOCS-1 expression, and HCV was analyzed. The lowest expression of SOCS-1 was observed in HCV-HCC tissues. Tissues with a higher HCV viral load showed lower SOCS-1 expression (p = 0.0282). Consistently, SOCS-1 mRNA and protein were lower in HCV-replicating cell lines than in uninfected ones. Furthermore, gene methylation was found in all examined tissues but higher in HCC tissues, and it is positively correlated with HCV viral load (r2 = 0.7309, p < 0.0001). HCV infection would upregulate methylation of the SOCS-1 gene in HCV-replicating cell lines. The downregulation of SOCS-1 in normal and HCV-replicating cell lines may result from HCV infection through epigenetic regulation, in which gene methylation in the CpG island of SOCS-1 promoters upon HCV infection suppresses its expression.

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MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

Cited by 15 publications

References 44 publications

Circulating miR-155 and JAK2/STAT3 Axis in Acute Ischemic Stroke Patients and Its Relation to Post-Ischemic Inflammation and Associated Ischemic Stroke Risk Factors

Circulating miR-155 and JAK2/STAT3 Axis in Acute Ischemic Stroke Patients and Its Relation to Post-Ischemic Inflammation and Associated Ischemic Stroke Risk Factors

LncRNA MALAT1 Participates in Protection of High-Molecular-Weight Hyaluronan against Smoke-Induced Acute Lung Injury by Upregulation of SOCS-1

CpG Island Methylation of Suppressor of Cytokine Signaling-1 Gene Induced by HCV Is Associated With HCV-Related Hepatocellular Carcinoma

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