MiR‐16, as a potential NF‐κB‐related miRNA, exerts anti‐inflammatory effects on LPS‐induced myocarditis via mediating CD40 expression: A preliminary study

Li, Qiang‐Qiang; Xi, Jing; Li, Bingqiang; Li, Ning

doi:10.1002/jbt.22426

Cited by 15 publications

(9 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that miR-16 can induce the expression of CD40 to play anti-inflammatory role in LPS-induced myocarditis [14]. Consistently, our study showed that miR-16 played inhibitory effects on the apoptosis of cardiomyocyte-induced by LPS.…”

Section: Discussionsupporting

confidence: 89%

“…It has been well established that many, noncoding RNAs (ncRNAs), such as miRNAs and long ncRNAs (> 200nt, lncRNAs) are involved in LPSmediated inflammation [12], indicating their potential involvement in sepsis. Previous studies have showed that lncRNA CAIF and miR-16 could inhibit LPS-induced inflammatory response [13,14]. This study was therefore carried out to investigate the interactions between CAIF and miR-16 in sepsis.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

LncRNA CAIF Upregulates miR-16 Through Methylation to Suppress LPS-Induced Apoptosis of Cardiomyocytes

Wang¹,

Zhang²

2020

Preprint

View full text Add to dashboard Cite

Background: Both lncRNA CAIF and miR-16 can inhibit LPS-induced inflammatory response. It is known that LPS plays crucial roles in sepsis. This study was therefore carried out to investigate the interactions between CAIF and miR-16 in sepsis.Methods: Levels of CAIF (A) and miR-16 (B) in plasma samples from sepsis patients (n = 60) and healthy controls (n = 60) were measured by performing RT-qPCR. Correlations of levels of CAIF and miR-16 across plasma samples from sepsis patients (A) and healthy controls (B) were analyzed by linear regression.The effects of CAIF overexpression on miR-16 (B), and the effects of miR-16 overexpression on CAIF (C) were analyzed by RT-qPCR.Results: We found that CAIF and miR-16 were downregulated in plasma of sepsis patients and they were positively correlated. In cardiomyocytes, LPS treatment led to downregulated CAIF and miR-16. Moreover, CAIF overexpression led to upregulated miR-16 and increased methylation of miR-16. However, miR-16 overexpression failed to significantly affect CAIF expression. Cell apoptosis analysis showed that CAIF and miR-16 overexpression suppressed LPS-induced apoptosis of cardiomyocytes. The combination of CAIF and miR-16 overexpression showed stronger effect.Conclusion: CAIF may upregulate miR-16 through methylation to suppress LPS-induced apoptosis of cardiomyocytes.

show abstract

Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

LncRNA CAIF Upregulates miR-16 Through Methylation to Suppress LPS-Induced Apoptosis of Cardiomyocytes

Wang¹,

Zhang²

2020

Preprint

View full text Add to dashboard Cite

show abstract

“… 59 Besides, miR-16 could mediate the expression of CD40 and inhibit the NF-κB signaling pathway to alleviate LPS-induced myocardial cell injury. 60 Thus, these above-mentioned results should promote further in-depth investigation of HLHS mechanism by which specific miRNAs dysregulate mitochondrial dysfunction via NF-κB signaling.…”

Section: Discussionmentioning

confidence: 94%

Integrative Bioinformatics Analysis Revealed Mitochondrial Defects Underlying Hypoplastic Left Heart Syndrome

Zhao¹,

Liu²,

Xu³

et al. 2021

IJGM

View full text Add to dashboard Cite

Background Hypoplastic left heart syndrome (HLHS) is one of the most complex congenital cardiac malformations, and the molecular mechanism of heart failure (HF) in HLHS is still elusive. Methods Integrative bioinformatics analysis was performed to unravel the underlying genes and mechanisms involved in HF in HLHS. Microarray dataset GSE23959 was screened out for the differentially expressed genes (DEGs), after which the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses were carried out using the Metascape. The protein–protein interaction (PPI) network was generated, and the modules and hub genes were identified with the Cytoscape-plugin. And the integrated network of transcription factor (TF)-DEGs and miRNA-DEGs was constructed, respectively. Results A total of 210 DEGs were identified, including 135 up-regulated and 75 down-regulated genes. The functional enrichment analysis of DEGs pointed towards the mitochondrial-related biological processes, cellular components, molecular functions and signaling pathways. A PPI network was constructed including 155 nodes as well as 363 edges. And 15 hub genes, such as NDUFB6, UQCRQ, SDHD, ATP5H , were identified based on three topological analysis methods and mitochondrial components and functions were the most relevant. Furthermore, by integrating network interaction construction, 23 TFs (NFKB1, RELA, HIF1A, VHL, GATA1, PPAR-γ, etc.) as well as several miRNAs (hsa-miR-155-5p, hsa-miR-191-5p, hsa-mir-124-3p, hsa-miR-1-3p, etc.) were detected and indicated the possible involvement of NF-κB signaling pathways in mitochondrial dysfunction in HLHS. Conclusion The present study applied the integrative bioinformatics analysis and revealed the mitochondrial-related key genes, regulatory pathways, TFs and miRNAs underlying the HF in HLHS, which improved the understanding of disease mechanisms and the development of novel therapeutic targets.

show abstract

“…64 In TB patients, miR-16 is significantly elevated but miR-155 is reduced. 65 While TLR4 stimulation reduces the level of miR-16 that negatively regulates the CD40 expression, 66 Helicobacter pylori infection enhances the expression of miR-155 that promotes CD40 and TNF-a expression. 67 Thus, Mtb infection modulates the expression of miR-16, miR-21, miR-29a, miR-145, miR-146a and miR-155, which in turn regulate CD40 expression ( Figure 3).…”

Section: Mycobacterial Alteration Of Host Micrornamentioning

confidence: 99%

March of Mycobacterium: miRNAs intercept host cell CD40 signalling

Chauhan

Dandapat

Sarkar³

et al. 2020

Clin & Trans Imm

View full text Add to dashboard Cite

The disease tuberculosis is fatal if untreated. It is caused by the acid-fast bacilli Mycobacterium tuberculosis. Mycobacterium resides and replicates within the alveolar macrophages, causing inflammation and granuloma, wherein macrophage-T cell interactions enhance the inflammation-causing pulmonary caseous lesions. The first interactions between Mycobacterium and the receptors on macrophages decide the fate of Mycobacterium because of phagolysosomal impairments and the expression of several miRNAs, which may regulate CD40 expression on macrophages. While the altered phagolysosomal functions impede antigen presentation to the T cell-expressed antigen receptor, the interactions between the macrophage-expressed CD40 and the T cell-expressed CD40-ligand (CD40L or CD154) provide signals to T cells and Mycobacterium-infected macrophages. These two functions significantly influence the resolution or persistence of Mycobacterium infection. CD40 controls T-cell polarisation and host-protective immunity by eliciting interleukin-12p40, nitric oxide, reactive oxygen species and IFN-c production. Indeed, CD40deficient mice succumb to low-dose aerosol infection with Mycobacterium because of deficient interleukin (IL)-12 production leading to impaired IFN-c-secreting T-cell response. In contrast, despite generating fewer granulomas, the CD40L-deficient mice developed anti-mycobacterial T-cell responses to the levels observed in the wild-type mice. These host-protective responses are significantly subdued by the Mycobacterium-infected macrophage produced TGF-b and IL-10, which promote promycobacterial T-cell responses. The CD40-CD40L-induced counteractive immune responses against Mycobacterium thus present a conundrum that we explain here with a reconciliatory hypothesis. Experimental validation of the hypothesis will provide a rationale for designing anti-tubercular immunotherapy.

show abstract

MiR‐16, as a potential NF‐κB‐related miRNA, exerts anti‐inflammatory effects on LPS‐induced myocarditis via mediating CD40 expression: A preliminary study

Cited by 15 publications

References 40 publications

LncRNA CAIF Upregulates miR-16 Through Methylation to Suppress LPS-Induced Apoptosis of Cardiomyocytes

LncRNA CAIF Upregulates miR-16 Through Methylation to Suppress LPS-Induced Apoptosis of Cardiomyocytes

Integrative Bioinformatics Analysis Revealed Mitochondrial Defects Underlying Hypoplastic Left Heart Syndrome

March of Mycobacterium: miRNAs intercept host cell CD40 signalling

Contact Info

Product

Resources

About