Effect of gga-miR-155 on cell proliferation, apoptosis and invasion of Marek’s disease virus (MDV) transformed cell line MSB1 by targeting RORA

Ding, Ke; Zhao, Yu; Chen, Yu; Jia, Yushan; He, Lei; Liao, Chengshui; Li, Jing; Zhang, Chunjie; Li, Yingju; Wu, Tingcai; Xiao, Cheng; Zhou, Zhiyu; Yu, Zuling

doi:10.1186/s12917-020-2239-4

Cited by 13 publications

(7 citation statements)

References 51 publications

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“…PPARD knockdown decreased the expression of 39 genes by less than or equal to 0.5-fold ( Table 2 ). Among these genes, LPAR3 , GAL3ST1 , PTPN11 , and RORA are involved in apoptosis [ 29 , 30 , 31 , 32 ]. We examined the effect of Cd on the expression of 15 of the above genes ( Figure 5 , data not shown).…”

Section: Resultsmentioning

confidence: 99%

Cadmium Toxicity Is Regulated by Peroxisome Proliferator-Activated Receptor δ in Human Proximal Tubular Cells

Mori

Lee

Tokumoto

et al. 2022

IJMS

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Cadmium (Cd) is a toxic heavy metal that is widely present in the environment. Renal proximal tubule disorder is the main symptom of Cd chronic poisoning. Our previous study demonstrated that Cd inhibits the total activities of peroxisome proliferator-activated receptor (PPAR) transcription factors in human and rat proximal tubular cells. In this study, we investigated the involvement of PPAR in Cd renal toxicity using the HK-2 human proximal tubular cell line. Among PPAR isoform genes, only PPARD knockdown significantly showed resistance to Cd toxicity in HK-2 cells. The transcriptional activity of PPARδ was decreased not only by PPARD knockdown but also by Cd treatment. DNA microarray analysis showed that PPARD knockdown changed the expression of apoptosis-related genes in HK-2 cells. PPARD knockdown decreased apoptosis signals and caspase-3 activity induced by Cd treatment. PPARD knockdown did not affect the intracellular Cd level after Cd treatment. These results suggest that PPARδ plays a critical role in the modification of susceptibility to Cd renal toxicity and that the apoptosis pathway may be involved in PPARδ-related Cd toxicity.

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Section: Resultsmentioning

confidence: 99%

Cadmium Toxicity Is Regulated by Peroxisome Proliferator-Activated Receptor δ in Human Proximal Tubular Cells

Mori

Lee

Tokumoto

et al. 2022

IJMS

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“…Many viral genes in MDV genome have been identified that may involve in MD development, such as, meq [ 47 ], viral telomerase RNA (vTR) [ 48 ], viral interleukin-8 (vIL-8) [ 49 ], phosphoprotein 38 (pp38) [ 50 , 51 ], and MDV miRNAs [ 52 ]. For host genome, some genes involved in MD pathogenies were identified, including MHC [ 27 , 53 ], gga-miR-155 [ 54 ], gga-miR-26a and NEK6 [ 55 ], IGFBP7 and TNFRSF8 [ 39 ]. Several studies also illustrated the mechanism of susceptive or resistance from the epigenomic level [ 56 , 57 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

Exploration of Alternative Splicing (AS) Events in MDV-Infected Chicken Spleens

Wang

Zheng

Yuan

et al. 2021

Genes

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Marek’s disease (MD) was an immunosuppression disease induced by Marek’s disease virus (MDV). MD caused huge economic loss to the global poultry industry, but it also provided an ideal model for studying diseases induced by the oncogenic virus. Alternative splicing (AS) simultaneously produced different isoform transcripts, which are involved in various diseases and individual development. To investigate AS events in MD, RNA-Seq was performed in tumorous spleens (TS), spleens from the survivors (SS) without any lesion after MDV infection, and non-infected chicken spleens (NS). In this study, 32,703 and 25,217 AS events were identified in TS and SS groups with NS group as the control group, and 1198, 1204, and 348 differently expressed (DE) AS events (p-value < 0.05 and FDR < 0.05) were identified in TS vs. NS, TS vs. SS, SS vs. NS, respectively. Additionally, Function enrichment analysis showed that ubiquitin-mediated proteolysis, p53 signaling pathway, and phosphatidylinositol signaling system were significantly enriched (p-value < 0.05). Small structural variations including SNP and indel were analyzed based on RNA-Seq data, and it showed that the TS group possessed more variants on the splice site region than those in SS and NS groups, which might cause more AS events in the TS group. Combined with previous circRNA data, we found that 287 genes could produce both circular and linear RNAs, which suggested these genes were more active in MD lymphoma transformation. This study has expanded the understanding of the MDV infection process and provided new insights for further analysis of resistance/susceptibility mechanisms.

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“…MicroRNAs (miRNAs), as 19-22 nucleotide non-coding RNAs, involve in multiple important biological processes by binding partially complementary sequences of its target gene mRNA 3'-untanslated region (3'-UTR) and repressing target gene functions. Many studies have demonstrated that miRNAs play important roles in resisting kinds of disease in birds, like Marek's disease virus, avian in uenza virus, bursal disease virus and others virus infection [6][7][8]. Our previous studies have also highlighted the critical role of miRNAs during MG-HS (Mycoplasma gallisepticum-Huangshi) infection in lung tissue of chicken embryo, including miR-19a, miR-130b-3p, miR-451 ect [9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 88%

Exosomal miR-181a-5p Protects against MG Infection by Targeting PPM1B and Activating the TLR2-Mediated MyD88/NF-κB Pathway

Sun¹,

Zhao²,

Pang³

et al. 2020

Preprint

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BackgroundMycoplasma gallisepticum (MG) is one of the most important pathogens that causes chronic respiratory disease (CRD) in chickens. Exosomes secreted from cells have been well documented to deliver miRNAs to recipient cells to modulate cellular function. The purpose of this current study was to explore the functions of exosomal miR-181a-5p in MG infection and the underlying mechanisms. ResultsHere, we found that miR-181a-5p expression in vivo and in vitro was significantly upregulated after MG infection. Exosomes enriched in MG-infected chicken type-II pneumocytes (CP-II) could selectively load miR-181a-5p and transfer it into recipient DF-1 cells. PPM1B was further identified as the target gene of miR-181a-5p. Overexpression of miR-181a-5p and/or knockdown of PPM1B activated the TLR2-mediated MyD88/NF-κB signaling pathways, whereas inhibition of miR-181a-5p and the overexpression of PPM1B led to the opposite results. In addition, depressing miR-181a-5p significantly reduced the expression of tumor necrosis factors alpha (TNF-α) and interleukin-1β (IL-1β) by MG-induced. Upregulated miR-181a-5p promoted cell proliferation and cell cycle progression and inhibited apoptosis to resist MG infection. Moreover, overexpression of miR-181a-5p significantly depressed pMAG1.2 expression by directly inhibiting PPM1B.ConclusionsTaken together, we conclude that the newly identified primary CP-II cells exosomal miR-181a-5p activates the TLR2-mediated MyD88/NF-κB pathway by directly targeting PPM1B to promote pro-inflammatory cytokines expression for defending against MG infection in recipient DF-1 cells.

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Effect of gga-miR-155 on cell proliferation, apoptosis and invasion of Marek’s disease virus (MDV) transformed cell line MSB1 by targeting RORA

Cited by 13 publications

References 51 publications

Cadmium Toxicity Is Regulated by Peroxisome Proliferator-Activated Receptor δ in Human Proximal Tubular Cells

Cadmium Toxicity Is Regulated by Peroxisome Proliferator-Activated Receptor δ in Human Proximal Tubular Cells

Exploration of Alternative Splicing (AS) Events in MDV-Infected Chicken Spleens

Exosomal miR-181a-5p Protects against MG Infection by Targeting PPM1B and Activating the TLR2-Mediated MyD88/NF-κB Pathway

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