Project description:The study profiles genome-wide miRNA expression in blood from 15 early-onset SZ (EOS) cases and 15 healthy controls. A total of 1070 miRNAs were detected by the microarrays in our samples. We profiles miRNA expression in 15 schizophrenia samples and 15 healthy controls to explore the alteration of miRNAs in schizophrenia.
Project description:Expression of interleukin-15 (IL-15) on the surface of human graft endothelial cells (ECs) bound to the IL-15 receptor a (IL-15Ra) subunit can increase the activation of cytotoxic T lymphocytes (CTLs), potentiating allograft rejection. Our previous work showed that surface expression of this protein complex could be induced by alloantibody-mediated complement activation through increased IL-1b synthesis, secretion, and autocrine/paracrine IL-1-mediated activation of NF-kB. Here we report that cultured human ECs express 8 differently spliced IL-15 transcripts. Remarkably, IL-1β does not alter the expression level of any IL-15 transcript but induces surface expression independently of RNA Polymerase II-mediated transcription while requiring new protein translation. Mechanistically, IL-1β causes an NF-kB-mediated reduction in the level of microRNA Let-7c-3p, thereby relieving a block of translation of IL-15 surface protein. Let7c-3p antimir can induce EC surface expression of IL-15/IL-15Ra in the absence of complement activation or of IL-1, enabling IL-15 trans-presentation to boost CD8 T cell activation. Because of the complexity we have uncovered in IL-15 regulation, we recommend caution in interpreting increased total IL-15 mRNA or protein levels as a surrogate for trans-presentation.
