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UV irradiated C. elegans

ABSTRACT: UV irradiated C. elegans

PROVIDER: PRJNA563824 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10065400.fastq.gz	Fastqsanger.gz
	SRR10065377_1.fastq.gz	Fastqsanger.gz
	SRR10065377_2.fastq.gz	Fastqsanger.gz
	SRR10065378_1.fastq.gz	Fastqsanger.gz
	SRR10065378_2.fastq.gz	Fastqsanger.gz

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Project description:UV-induced CPDs were mapped in primary skin melanocytes or normal human skin fibroblasts following either UVC or UVB irradiation and in isolated human genomic DNA (naked DNA control) that was UVB or UVC irradiated. CPDs were mapped across the human genome using the CPD-capture-seq method and the resulting libraries were captured for ~4000 genomic regions of interest (~3 Mbp) of the human genome by the company Rapid Genomics prior to Illumina sequencing

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Reticulon-1 and reduced migration towards chemoattractants by macrophages differentiated from the bone marrow of UV-irradiated and UV-chimeric mice

Project description:The ability of macrophages to respond to chemoattractants and inflammatory signals is important for their migration to sites of inflammation and immune activity and for host responses to infection. Macrophages differentiated from the bone marrow of UV-irradiated mice, even after activation with LPS, migrated inefficiently towards CSF-1 and CCL2. When bone marrow cells were harvested from UV-irradiated mice, and transplanted into naïve mice, the recipient mice (UV-chimeric) had reduced accumulation of elicited macrophages in the peritoneal cavity in response to inflammatory thioglycollate or alum. Macrophages differentiating from the bone marrow of UV-chimeric mice also had an inherent reduced ability to migrate towards chemoattractants in vitro, even after LPS activation. Microarray analysis identified reduced reticulon-1 mRNA in macrophages differentiated from the bone marrow of UV-chimeric mice. By using an anti-reticulon-1 antibody, a role for reticulon-1 in macrophage migration was confirmed. The proposal that reduced reticulon-1 is responsible for the poor inherent ability of macrophages to respond to chemokine gradients was supported by Western blotting. In summary, skin exposure to erythemal UV radiation can modulate macrophage progenitors in the bone marrow such that the properties of their differentiated progeny respond inefficiently to signals to accumulate at sites of inflammation and immunity.

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