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MRNA expression profiling analysis obtained from meninges of PRELP knockout mouse

ABSTRACT: mRNA expression profiling analysis obtained from meninges of PRELP knockout mouse

PROVIDER: PRJNA818617 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18429424_1.fastq.gz	Fastqsanger.gz
	SRR18429424_2.fastq.gz	Fastqsanger.gz
	SRR18429425_1.fastq.gz	Fastqsanger.gz
	SRR18429425_2.fastq.gz	Fastqsanger.gz
	SRR18429426_1.fastq.gz	Fastqsanger.gz

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mRNA expression profiling analysis obtained from meninges of PRELP knockout mouse

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Project description:The meninges are generally considered relatively inert tissues that house the CSF and provide protection for the brain and spinal cord. However, our previous studies using Kit mutant (Kit W/Wv) mast cell-deficient mice demonstrated that mast cells residing in the dura mater and pia mater exacerbate the severity of experimental autoimmune encephalomyelitis (EAE), the rodent model of the CNS demyelinating disease, multiple sclerosis. These data suggest that the meninges are sites of active immune responses in disease. Gene expression profiles of meningeal tissue from wild type and mast cell deficient mice prior to and at day 6 post-EAE induction were found highly distinct. Increases in both mast cell- and neutrophil-associated transcripts were among the notable disease-related changes observed in wild type mice. Kinetic analyses show that meningeal mast cells are activated within 24 hours of disease induction to express multiple mediators including IL-1b and TNF as well as the neutrophil chemoattractant, CXCL2, an observation corresponding with an influx of neutrophils to the meninges. Neutrophil recruitment as well as the disease-related loss of BBB integrity is dependent on mast cell-derived TNF. These data provide unequivocal evidence that the meninges are sites of early inflammatory events in EAE. Mast cells residing within these tissues promote disease by orchestrating an early and efficient immune cell co-localization resulting in a robust local inflammatory response and a breach of the proximal BBB. We hypothesize that these events reflect an aberrant manifestation of the normal immune surveillance role of the meninges in infection settings.

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Project description:Two secreted proteins, osteomodulin (OMD) and proline/arginine-rich end leucine repeat protein (PRELP), are specifically expressed in bladder epithelial umbrella cells. At the initiation of human bladder cancer, their expression levels are dramatically down-regulated. To reveal the functional role of both proteins in bladder cancer, we constructed OMD or PRELP knockout mice and found that, in bladder epithelia, tight junctions between umbrella cells are strongly reduced while adherens junctions are remained as observed as a typical partial epithelial-mesenchymal transition (EMT). In addition, OMD or PRELP knockout mouse bladder showed many spontaneous breakdown sites in the umbrella cell layer. Furthermore, a third of the PRELP-/- mice developed non-muscle invasive papillary bladder cancer (NMIBC). mRNA expression profiling and in vitro functional analysis revealed that OMD and PRELP strongly regulate cell-cell adhesion and EMT via tight junction regulation through inhibition of TGF-b and EGF pathways. Interestingly, we found that activation of OMD or PRELP in bladder cancer cells strongly inhibits anchorage independent growth in vitro and tumorigenicity in in vivo mouse xenograft studies associating with the transition from mesenchymal cancer cells to epithelial-like cells as well as with tight junctions. Our data indicate that OMD and PRELP are involved in NMIBC initiation through regulation of the transition between epithelial and mesenchymal cells. Thus, it suggests that OMD and/or PRELP mediated EMT may have a potential target for bladder cancer therapy.

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