MicroRNAs as master regulators of immune responses in transplant recipients

Kaul, Vandana; Krams, Sheri M.

doi:10.1097/mot.0000000000000148

Cited by 19 publications

(10 citation statements)

References 109 publications

(110 reference statements)

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“…On the other hand, some reports indicate that miRNA could directly regulate the expression of viral genes, thus interfering with viral replication. 4 , 16 Sonkoly et al 17 found a close link between miRNAs and a chronic inflammatory skin disease that indicates the important immunomodulatory effect of miRNAs. These findings also reflect the mechanism by which miRNA regulates viral infection.…”

Section: Discussionmentioning

confidence: 99%

miR-370 mimic inhibits replication of Japanese encephalitis virus in glioblastoma cells

Li¹,

Peng²,

Nie³

et al. 2016

NDT

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Japanese encephalitis (JE) is one of the most severe viral infections of the central nervous system. No effective treatment for JE currently exists, because its pathogenesis remains largely unknown. The present study was designed to screen the potential microRNAs (miRNAs) involved in JE. Glioblastoma cells were collected, after being infected with the Japanese encephalitis virus (JEV). Total miRNAs were extracted and analyzed using an miRNA chip. One of the most severely affected miRNAs was selected, and the role of miR-370 in JEV infection was investigated. Cell viability and apoptosis of the host cells were evaluated. JEV replication was detected via analysis of gene E expression. Real-time polymerase chain reaction was used to determine the levels of endogenous miR-370 and expression of innate immunity-related genes. Following JEV infection, 114 miRNAs were affected, as evidenced by the miRNA chip. Among them, 30 miRNAs were upregulated and 84 were downregulated. The changes observed in five miRNAs were confirmed by real-time polymerase chain reaction. One of the significantly downregulated miRNAs was miR-370. Therefore, miR-370 mimic was transfected into the cells, following which the levels of endogenous miR-370 were significantly elevated. Concurrently, JEV replication was significantly reduced 24 hours after transfection of miR-370 mimic. Functionally, miR-370 mimic mitigated both JEV-induced apoptosis and the inhibition of host cell proliferation. Following JEV infection, interferon-β and nuclear factor-kappa B were upregulated, whereas miR-370 mimic prevented the upregulation of the genes induced by JEV infection. The present study demonstrated that miR-370 expression in host cells is downregulated following JEV infection, which further mediates innate immunity-related gene expression. Taken together, miR-370 mimic might be useful to prevent viral replication and infection-induced host cell injury.

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Section: Discussionmentioning

confidence: 99%

miR-370 mimic inhibits replication of Japanese encephalitis virus in glioblastoma cells

Li¹,

Peng²,

Nie³

et al. 2016

NDT

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“…Further supporting this concept, serum miRNAs have been proposed as potential prognostic biomarkers in different transplantation settings [4,15,16]. Due to cohort constrains we were not able to assess potential correlations between the miRNAs investigated in this study and other biomarkers, including inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 78%

Serum miRNAs as Potential Biomarkers for the Bronchiolitis Obliterans Syndrome after Lung Transplantation

Budding

Rossato

Graaf

et al. 2016

The Journal of Heart and Lung Transplantation

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A B S T R A C TLung transplantation (LTx) is the last treatment for patients suffering from end-stage lung diseases. Survival postLTx is hampered by the development of the bronchiolitis obliterans syndrome (BOS) and diagnosis is often late. Given the urgent clinical need to recognize BOS patients at an early stage, we analyzed circulating miRNAs to identify possible stratification markers for BOS development post-transplantation. Therefore, pro-fibrotic (miR-21, miR-155), anti-fibrotic (miR-29a) and fibrosis-unrelated (miR-103, miR-191) miRNAs were analyzed in serum of end-stage lung disease patients and during LTx follow-up.Significant elevated levels of serum miRNAs were observed for all investigated miRNAs in both chronic obstructive pulmonary disease and interstitial lung disease patients compared to healthy controls. The same miRNAs were also significantly increased in the serum of BOS + vs. BOS− patients. Most importantly, miR-21, miR-29a, miR-103, and miR-191 levels were significantly higher in BOS+ patients prior to clinical BOS diagnosis.We demonstrated that a selected group of miRNAs investigated is elevated in end-stage lung disease and BOS + patients, prior to clinical BOS diagnosis. Even if further research is expedient on the prognostic value of circulating miRNAs in BOS and lung conditions in general, these results strongly suggest that circulating miRNAs could be used as potential biomarkers for BOS development.

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“…First, our findings demonstrated that miR-124-3p was downregulated in HG-stimulated HRMECs. MiRNAs are major regulators in a variety of diseases (Kaul and Krams, 2015;Trionfini and Benigni, 2017). Specially, it has been confirmed that miRNAs exert pivotal functions in the initiation and development of DR. For example, miR-138-5p exerts a protective role the early DR by regulating NOVA1 (Bao and Cao, 2019).…”

Section: Discussionmentioning

confidence: 97%

MiR-124-3p Suppresses the Dysfunction of High Glucose-Stimulated Endothelial Cells by Targeting G3BP2

Zhao

2021

Front. Genet.

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Background: Diabetic retinopathy (DR) is the most important manifestation of diabetic microangiopathy. MicroRNAs (miRNAs), members of non-coding RNAs, have been frequently reported to regulate various diseases including DR. MiR-124-3p is involved in DR based on bioinformatics. The current study aimed to investigate the role of miR-124-3p in high glucose (HG)-treated human retinal microvascular endothelial cells (HRMECs), an in vitro model of DR.Methods: Bioinformatics analysis was applied to reveal the targets downstream miR-124-3p. A series of assays including CCK-8, luciferase reporter, western blot, and tube formation assays were used to explore the function and mechanism of miR-124-3p in HG-stimulated HRMECs.Results: We found out that miR-124-3p was downregulated in HG-stimulated HRMECs. Functionally, miR-124-3p overexpression restrained the HG-induced cell injury of HRMECs. Mechanistically, we predicted 5 potential target mRNAs of miR-124-3p. G3BP stress granule assembly factor 2 (G3BP2) was validated to bind with miR-124-3p. Rescue assays showed that miR-124-3p suppressed cell injury of HG-stimulated HRMECs through G3BP2. In addition, miR-124-3p regulated the p38MAPK signaling pathway by G3BP2, and G3BP2 promoted injury of HG-treated HRMECs through the activation of the p38MAPK signaling pathway.Conclusion: MiR-124-3p suppressed the dysfunctions of HG-treated HRMECs by targeting G3BP2 and activating the p38MAPK signaling. This new discovery provided a potential biomarker for DR treatment.

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MicroRNAs as master regulators of immune responses in transplant recipients

Abstract: miRNA-based diagnosis is a fast-moving field with new miRNA signatures being identified each day. Recent advances have also been successful at taking a few of these miRNAs to clinical trials for therapeutic interventions.

Cited by 19 publications

References 109 publications

miR-370 mimic inhibits replication of Japanese encephalitis virus in glioblastoma cells

miR-370 mimic inhibits replication of Japanese encephalitis virus in glioblastoma cells

Serum miRNAs as Potential Biomarkers for the Bronchiolitis Obliterans Syndrome after Lung Transplantation

MiR-124-3p Suppresses the Dysfunction of High Glucose-Stimulated Endothelial Cells by Targeting G3BP2

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