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Gene expression comparison of microRNA-181d Transgenic and microRNA-181d Knock-in thymocytes

ABSTRACT: T cell-specific over-expression of microRNA-181d reduced number of immature CD4+CD8+ thymocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE50113 | GEO | 2014/02/20

SECONDARY ACCESSION(S): PRJNA217048

REPOSITORIES: GEO

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Gene expression comparison of microRNA-181d Transgenic and microRNA-181d Knock-in thymocytes

Project description:T cell-specific over-expression of microRNA-181d reduced number of immature CD4+CD8+ thymocytes. Whole thymus tissues were isolated from the miR-181d transgenic (Tg-8) and miR-181d knockin (KI) mice, followed by total RNA isolation.

2014-02-20 | E-GEOD-50113 | biostudies-arrayexpress

Identification of the molecular targets of microRNA-181d in murine thymocytes.

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Identification of the molecular targets of microRNA-181d in murine thymocytes.

Project description:T cell-specific transgenic expression of microRNA-181d reduced number of immature CD4+CD8+ thymocytes. Microarray analysis was performed to reveal differentially expressed genes between the wild type and microRNA-181d transgenic thymocytes. Whole thymus tissues were isolated from the wild type (C57BL/6) and microRNA-181d transgenic mice (Tg-38 line), followed by total RNA isolation.

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Transgenic expression of microRNA-181d augments the stress-sensitivity of CD4(+)CD8(+) thymocytes.

Project description:Physiological stress resulting from infections, trauma, surgery, alcoholism, malnutrition, and/or pregnancy results in a substantial depletion of immature CD4(+)CD8(+) thymocytes. We previously identified 18 distinct stress-responsive microRNAs (miRs) in the thymus upon systemic stress induced by lipopolysaccharide (LPS) or the synthetic glucocorticoid, dexamethasone (Dex). MiRs are short, non-coding RNAs that play critical roles in the immune system by targeting diverse mRNAs, suggesting that their modulation in the thymus in response to stress could impact thymopoiesis. MiR-181d is one such stress-responsive miR, exhibiting a 15-fold down-regulation in expression. We utilized both transgenic and gene-targeting approaches to study the impact of miR-181d on thymopoiesis under normal and stress conditions. The over-expression of miR-181d in developing thymocytes reduced the total number of immature CD4(+)CD8(+) thymocytes. LPS or Dex injections caused a 4-fold greater loss of these cells when compared with the wild type controls. A knockout mouse was developed to selectively eliminate miR-181d, leaving the closely spaced and contiguous family member miR-181c intact. The targeted elimination of just miR-181d resulted in a thymus stress-responsiveness similar to wild-type mice. These experiments suggest that one or more of three other miR-181 family members have overlapping or compensatory functions. Gene expression comparisons of thymocytes from the wild type versus transgenic mice indicated that miR-181d targets a number of stress, metabolic, and signaling pathways. These findings demonstrate that selected miRs enhance stress-mediated thymic involution in vivo.

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Cyclic stretch-induced exosomes from periodontal ligament cells promote osteoblasts osteogenic differentiation via the miR-181d-5p/TNF signaling pathway

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Gene expression profiling in mature OT-II TCR transgenic CD4 SP thymocytes, either Jmjd3- and Utx-deficient or -sufficient.

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