Efficient growth cone regeneration requires protein synthesis in the adult mammalian brain and spinal cord. Recent evidence suggests that the local availability of protein synthesis machinery in adult mammalian axons may be an indicator of their regenerative capacity. Here we investigated the local protein synthesis capacity in matured cortical axons, which have poor regenerative capacity, yet are critical for recovery following injury due to traumatic brain injury and stroke. This work is the first to biochemically isolate and identify mRNA from mammalian cortical axons, making use of a unique microfluidic platform to isolate axons free of other cellular debris. We first sought to identify mRNA in nave axons that makes up the pool of mRNA available for translation initiated following axotomy. Next, we investigated changes in the mRNA population localized to axons 2 days following axotomy and growth cone regeneration.
Axonal mRNA in uninjured and regenerating cortical mammalian axons.
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View SamplesTo determine whether P. aeruginosa strain PA14 exhibits a specific transcriptional response to extracellular Fe(II), a microarray experiment was performed using Affymetrix GeneChips. The transcriptional response to Fe(II) or Fe(III) shock was measured and compared to a no-Fe control.
BqsR/BqsS constitute a two-component system that senses extracellular Fe(II) in Pseudomonas aeruginosa
Compound
View SamplesMammalian microRNAs (miRNAs) are emerging as key regulators of the development and function of the immune system. Here, we report a strong but transient induction of miR-155 in mouse bone marrow after injection of bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating the sufficiency of miR-155 to drive GM expansion, enforced expression in mouse bone marrow cells caused GM proliferation in a manner reminiscent of LPS treatment. However, the mir-155-induced GM populations displayed pathological features characteristic of myeloid neoplasia. Extending possible relevance to human disease, miR-155 was overexpressed in the bone marrow of patients with acute myeloid leukemia (AML). Furthermore, miR-155 repressed a subset of genes implicated in hematopoietic development and disease. These data implicate miR-155 as a contributor to physiological GM expansion during inflammation and to certain pathological features associated with AML, emphasizing the importance of proper miR-155 regulation in developing myeloid cells during times of inflammatory stress.
Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorder.
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View SamplesWe used microarrays to look at overall gene expression differences between miR-155-/- and WT dendritic cells under inflammatory conditions.
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