<i>Cryptosporidium parvum</i>Induces B7‐H1 Expression in Cholangiocytes by Down‐Regulating MicroRNA‐513

Gong, Ai Yu; Zhou, Rui; Hu, Guoku; Liu, Jun; Sоsnowska, Danuta; Drescher, Kristen M.; Dong, Haidong; Chen, Xian Ming

doi:10.1086/648589

Cited by 65 publications

(67 citation statements)

References 35 publications

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“…This leads to an increase of B7-H1 expressed on the cell surface that in vitro induces the apoptosis of activated T cells. 73 This is of particular interest because it illustrates the feasibility that parasites take advantage of host miRNA pathways as a method of defense against the host. The in vivo events following increased B7-H1 will be of interest to be further investigated.…”

Section: Disclosure Of Potential Conflicts Of Interestmentioning

confidence: 99%

microRNAs in parasites and parasite infection

2013

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Section: Disclosure Of Potential Conflicts Of Interestmentioning

confidence: 99%

microRNAs in parasites and parasite infection

2013

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“…Moreover, downregulation of miR-513 is required for upregulation of B7-H1 protein level in human biliary epithelial cells following IFN-γ stimulation or microbial challenge, suggesting a role of miR-513 in regulating biliary inflammatory responses through targeting of B7-H1. 66,67 …”

Section: Regulation Of Epithelial Immune Responses By Mirnasmentioning

confidence: 99%

MicroRNA regulation of innate immune responses in epithelial cells

2011

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Mucosal surface epithelial cells are equipped with several defense mechanisms that guard against pathogens. Recent studies indicate that microRNAs (miRNAs) mediate post-transcriptional gene suppression and may be a critical component of the complex regulatory networks in epithelial immune responses. Transcription of miRNA genes in epithelial cells can be elaborately controlled through pathogen recognition receptors, such as Toll-like receptors (TLRs), and associated nuclear factor kappaB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, and ultimately nuclear transcription factor associated-transactivation and transrepression. Activation of these intracellular signaling pathways may also modulate the process of miRNA maturation. Functionally, miRNAs may modulate epithelial immune responses at every step of the innate immune network, including production and release of cytokines/chemokines, expression of adhesion and costimulatory molecules, shuttling of miRNAs through release of exosomes and feedback regulation of immune homeostasis. Therefore, miRNAs act as critical regulators to the fine-tuning of epithelial immune responses.

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“…Several recent studies indicate that miRs may modulate TLR-mediated immune responses including production and release of cytokines and chemokines [17]–[19], expression of adhesion and co-stimulatory molecules [17], [20], and feedback regulation of immune responses [17], [18], [21]. miRs are endogenous, small (19–23 nucleotides long) single-stranded noncoding RNA that suppress gene expression either via translational inhibition or mRNA degradation (or both) and have emerged as key post-transcriptional regulators of gene expression [22]–[26].…”

Section: Introductionmentioning

confidence: 99%

TLR3-Induced Placental miR-210 Down-Regulates the STAT6/Interleukin-4 Pathway

et al. 2013

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Several clinical studies have reported increased placental miR-210 expression in women with PE compared to normotensive women, but whether miR-210 plays a role in the etiology of PE is unknown. We reported that activation of TLR3 produces the PE-like symptoms of hypertension, endothelial dysfunction, and proteinuria in mice only when pregnant, but whether TLR3 activation in pregnant mice and human cytotrophoblasts (CTBs) increases miR-210 and modulates its targets related to inflammation are unknown. Placental miR-210 levels were increased significantly in pregnant mice treated with the TLR3 agonist poly I:C (P-PIC). Both HIF-1α and NF-κBp50, known to bind the miR-210 promoter and induce its expression, were also increased significantly in placentas of P-PIC mice. Target identification algorithms and gene ontology predicted STAT6 as an inflammation-related target of miR-210 and STAT6 was decreased significantly in placentas of P-PIC mice. IL-4, which is regulated by STAT6 and increases during normotensive pregnancy, failed to increase in serum of P-PIC mice. P-PIC TLR3 KO mice did not develop hypertension and placental HIF-1α, NF-κBp50, miR-210, STAT6, and IL-4 levels were unchanged. To determine the placental etiology, treatment of human CTBs with poly I:C significantly increased HIF-1α, NF-κBp50, and miR-210 levels and decreased STAT6 and IL-4 levels. Overexpression of miR-210 in CTBs decreased STAT6 and IL-4 while inhibition of miR-210 increased STAT6 and IL-4. These findings demonstrate that TLR3 activation induces placental miR-210 via HIF-1α and NF-κBp50 leading to decreased STAT6 and IL-4 levels and this may contribute to the development of PE.

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Cryptosporidium parvumInduces B7‐H1 Expression in Cholangiocytes by Down‐Regulating MicroRNA‐513

Cited by 65 publications

References 35 publications

microRNAs in parasites and parasite infection

microRNAs in parasites and parasite infection

MicroRNA regulation of innate immune responses in epithelial cells

TLR3-Induced Placental miR-210 Down-Regulates the STAT6/Interleukin-4 Pathway

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