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Transcriptomic Signatures of Neuronally-Derived Extracellular Vesicles Reveals Presence of Olfactory Receptors in Clinical Samples of Traumatic Brain Injury Patients

ABSTRACT: Transcriptomic Signatures of Neuronally-Derived Extracellular Vesicles Reveals Presence of Olfactory Receptors in Clinical Samples of Traumatic Brain Injury Patients

PROVIDER: PRJNA1072136 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27840800_1.fastq.gz	Fastqsanger.gz
	SRR27840800_2.fastq.gz	Fastqsanger.gz
	SRR27840801_1.fastq.gz	Fastqsanger.gz
	SRR27840801_2.fastq.gz	Fastqsanger.gz
	SRR27840802_1.fastq.gz	Fastqsanger.gz

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Transcriptomic Signatures of Neuronally-Derived Extracellular Vesicles Reveals Presence of Olfactory Receptors in Clinical Samples of Traumatic Brain Injury Patients

Project description:Traumatic brain injury (TBI) is one of the major causes of death and disability worldwide. Recently, the FDA has approved blood-based biomarkers, GFAP and UCH-L1, to evaluate the need for CT scans, however, clinical translation is currently limited. Exosomes are small microcellular vesicles which are released from the cell in both normal and diseased states, as part of extracellular communication. The aim of this study was to isolate neuronal exosomes derived from the serum of patients with severe TBI and characterize the messenger RNA content of the exosomes released by the injured neurons in order to identify new potential blood-based biomarkers. RNA was isolated from neuronal exosomes and total transcriptomic sequencing was performed. RNA sequencing data from neuronal exosomes isolated from serum showed mRNA transcripts of several neuronal genes. Additionally, the RNA sequencing data revealed mRNA of several olfactory receptor genes, which were present at elevated concentrations in the neuronal exosomes. Further validation in serum samples of mild TBI patients revealed a similar upregulation of olfactory receptors. The data from these experiments suggests that damage to the neurons in the olfactory neuroepithelium and in the brain, following a TBI, may cause the release of mRNA from these receptors in the exosomes. Thus, olfactory receptors can be further investigated as potential biomarkers for TBI diagnosis.

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Transcriptomic Signatures of Neuronally Derived Extracellular Vesicles Reveal the Presence of Olfactory Receptors in Clinical Samples from Traumatic Brain Injury Patients.

Project description:Traumatic brain injury (TBI) is defined as an injury to the brain by external forces which can lead to cellular damage and the disruption of normal central nervous system functions. The recently approved blood-based biomarkers GFAP and UCH-L1 can only detect injuries which are detectable on CT, and are not sensitive enough to diagnose milder injuries or concussion. Exosomes are small microvesicles which are released from the cell as a part of extracellular communication in normal as well as diseased states. The objective of this study was to identify the messenger RNA content of the exosomes released by injured neurons to identify new potential blood-based biomarkers for TBI. Human severe traumatic brain injury samples were used for this study. RNA was isolated from neuronal exosomes and total transcriptomic sequencing was performed. RNA sequencing data from neuronal exosomes isolated from serum showed mRNA transcripts of several neuronal genes. In particular, mRNAs of several olfactory receptor genes were present at elevated concentrations in the neuronal exosomes. Some of these genes were OR10A6, OR14A2, OR6F1, OR1B1, and OR1L1. RNA sequencing data from exosomes isolated from CSF showed a similar elevation of these olfactory receptors. We further validated the expression of these samples in serum samples of mild TBI patients, and a similar up-regulation of these olfactory receptors was observed. The data from these experiments suggest that damage to the neurons in the olfactory neuroepithelium as well as in the brain following a TBI may cause the release of mRNA from these receptors in the exosomes. Hence, olfactory receptors can be further explored as biomarkers for the diagnosis of TBI.

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Project description:Olfactory sensory neurons (OSNs) are functionally defined by their expression of a unique odorant receptor (OR). Mechanisms underlying singular OR expression are well studied, and involve a massive cross-chromosomal enhancer interaction network. Trace amine-associated receptors (TAARs) form a distinct family of olfactory receptors, and here we find that mechanisms regulating Taar gene choice display many unique features. The epigenetic signature of Taar genes in TAAR OSNs is different from that in OR OSNs. We further identify that two TAAR enhancers conserved across placental mammals are absolutely required for expression of the entire Taar gene repertoire. Deletion of either enhancer dramatically decreases the expression probabilities of different Taar genes, while deletion of both enhancers completely eliminates the TAAR OSN populations. In addition, both of the enhancers are sufficient to drive transgene expression in the partially overlapped TAAR OSNs. We also show that the TAAR enhancers operate in cis to regulate Taar gene expression. Our findings reveal a coordinated control of Taar gene choice in OSNs by two remote enhancers, and provide an excellent model to study molecular mechanisms underlying formation of an olfactory subsystem.

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