Exosomes derived from plasma of septic patients inhibit apoptosis of T lymphocytes by down-regulating bad via hsa-miR-7-5p

Deng, Jian-nan; Li, Yanqin; Liu, Yang; Li, Qi; Hu, Ye; Xu, Jianqiao; Sun, Tianyu; Xie, Lixin

doi:10.1016/j.bbrc.2019.04.051

Cited by 32 publications

(36 citation statements)

References 26 publications

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“…miR-7-5p is relevant to vascular endothelial cell proliferation, glioma, brain damage, and cognitive dysfunction [66][67][68][69]. Moreover, it has been reported that miR-7-5p boosts apoptosis but inhibits cell proliferation and apoptosis of T lymphocytes, explaining the function of miR-214-3p and miR-7-5p in psoriasis [70,71]. It was reported that miR-1207-5p may exert an inhibitory effect on VEGF [72].…”

Section: Journal Of Immunology Researchmentioning

confidence: 99%

Plasma MicroRNA Expression Profiles in Psoriasis

Xiao

Liu

Wang

et al. 2020

Journal of Immunology Research

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Background. Psoriasis is an immune-mediated inflammatory chronic skin disease characterized by chronic inflammation in the dermis, parakeratosis, and excessive epidermal growth. MicroRNAs (miRNAs) are key regulators of immune responses. Although differential expression of miRNAs has been reported in certain inflammatory autoimmune diseases, their role in psoriasis has not been fully illuminated. Our aims were to confirm plasma miRNA expression signatures in psoriasis and to examine their potential influence on psoriasis pathogenesis. Methods. A miRNome PCR array was used to analyse the plasma of psoriasis patients and healthy donors. We performed miRNA pathway enrichment and target gene network analyses on psoriasis plasma samples. Results. We found several specific plasma miRNA signatures relevant to psoriasis. The miRNAs targeted pathways associated with psoriasis, such as the VEGF, MAPK, and WNT signaling pathways. Network analysis revealed pivotal deregulated plasma miRNAs and their relevant target genes and pathways regulating psoriasis pathogenesis. Conclusions. This study analysed the expression of plasma miRNAs and their target pathways, elucidating the pathogenesis of psoriasis; these results may be used to design novel therapeutic strategies and to identify diagnostic biomarkers for psoriasis.

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Section: Journal Of Immunology Researchmentioning

confidence: 99%

Plasma MicroRNA Expression Profiles in Psoriasis

Xiao

Liu

Wang

et al. 2020

Journal of Immunology Research

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“…It has also been shown that promoting the increase of miR-125 in sepsis can lead to the increase of T lymphocyte activity, immunoglobulin expression, and NK cell activity and inhibit the release of inflammatory factors and apoptosis of T lymphocyte [9]. hsa-miR-7-5p can also downregulate caspase-3 and upregulate Bcl-2 mRNA and protein, so as to inhibit LPSinduced apoptosis of T lymphocytes and reduce the mortality of septic mice [10]. In sepsis, miR-155 in lymphocytes promotes the inflammatory response of mice, leading to the progression of acute lung injury [11].…”

Section: Introductionmentioning

confidence: 99%

Influences of Regulation of miR-126 on Inflammation,Th17/Treg Subpopulation Differentiation, and Lymphocyte Apoptosis through Caspase Signaling Pathway in Sepsis

Zou

Yang

et al. 2020

Inflammation

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To observe the inflammatory response, differentiation of Th17/Treg subsets and apoptosis of lymphocytes, by regulating miR-126 in lymphocytes of septic rats. After using cecal ligation and puncture to establish sepsis model, miR-126 mimic and miR-126 inhibitor were used to transfect lymphocytes of septic rats in vitro and in vivo. ELISA was used to detect TNF-α, IL-6, IL-17, and IL-10, the differentiation of Th17 and Treg was measured by flow cytometry, and apoptosis of lymphocytes was observed by fluorescence microscope; the changes of caspase signaling pathway were detected by immunofluorescence, PCR, and Western blotting. The result show that the expression of miR-126 increased in sepsis. After overexpression of miR-126, the release of TNF-α, IL-6, and IL-17 decreased; the release of IL-10 increased; T lymphocyte subsets differentiated toward Treg; caspase signaling pathway weakened; and lymphocyte of apoptosis decreased compared with sepsis group. While, after inhibition of miR-126, the release of TNF-α, IL-6, and IL-17 increased; the release of IL-10 decreased; T lymphocyte subsets differentiated toward TH17; caspase signaling pathway enhanced; and lymphocyte of apoptosis increased compared with sepsis group. Taken together, regulation of miR-126 can alter the inflammatory response, differentiation of T lymphocyte subsets, and apoptosis of lymphocytes in septic rats.

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“…Overexpression of let-7 potentiates, whereas depletion of let-7 compromises, the LPS-induced inflammatory cytokine production [19]. It has been reported that miR-7-5p is required for the apoptotic inhibition of T lymphocytes and the immunosuppressive phenotypes in sepsis [20]. Low levels of serum miR-150 in sepsis patients predict unfavorable prognosis and a high ratio of organ dysfunction [21].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-19a Targets Fibroblast Growth Factor-Inducible Molecule 14 and Prevents Tubular Damage in Septic AKI

Hong

et al. 2020

Analytical Cellular Pathology

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Fibroblast growth factor-inducible molecule 14 (Fn14) plays a principal role in triggering tubular damage during septic acute kidney injury (AKI). Here, we explore the mechanism underlying Fn14 deregulation in septic AKI. We identify Fn14 as a bona fide target of miR-19a, which directly binds to 3′ UTR of Fn14 for repression independent of cylindromatosis (CYLD), the deubiquitinase (DUB) downstream of miR-19a, and thereby antagonizes the LPS-induced tubular cell apoptosis. Genetic ablation of Fn14, but not of CYLD, abolishes the ability of miR-19a to antagonize the tubular apoptosis by lipopolysaccharide (LPS). In mice, systemic delivery of miR-19a confers protection against septic AKI. Our findings implicate that miR-19a may serve as a promising therapeutic candidate in the prevention of septic AKI.

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Exosomes derived from plasma of septic patients inhibit apoptosis of T lymphocytes by down-regulating bad via hsa-miR-7-5p

Cited by 32 publications

References 26 publications

Plasma MicroRNA Expression Profiles in Psoriasis

Plasma MicroRNA Expression Profiles in Psoriasis

Influences of Regulation of miR-126 on Inflammation,Th17/Treg Subpopulation Differentiation, and Lymphocyte Apoptosis through Caspase Signaling Pathway in Sepsis

MicroRNA-19a Targets Fibroblast Growth Factor-Inducible Molecule 14 and Prevents Tubular Damage in Septic AKI

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