Dataset Information

Transcriptome Analysis of Dorsal Root Ganglion in Rats with Knee Joint Inflammation.

ABSTRACT:

Background

Rheumatoid arthritis (RA) leads to pain through alteration of gene expression. Although gene expression alteration in knee cartilage or peripheral blood from RA patients has been identified using microarray, it remains unclear whether long non-coding RNA (lncRNA)-mediated gene regulation occurs in primary sensory neurons of dorsal root ganglia (DRG) during RA-like joint inflammation. In the present study, we aimed to analyze lncRNA and related mRNA profiles in the DRG in a knee joint inflammation rat model.

Methods

Complete Freund's adjuvant (CFA) was injected in the rat knee joint for preparing the joint inflammation model. A lncRNA-mRNA microarray of rat DRG was employed for transcriptome analysis. Functional roles of differentially expressed lncRNAs and their related mRNAs in the injured DRG were delineated by bioinformatic analysis.

Results

We observed that expression levels of 9000 lncRNAs were altered on day 7 post-CFA, of which 45.17% were up-regulated and 54.83% were down-regulated. Specifically, 69 lncRNAs (42 up and 27 down) were significantly regulated. We also observed that expression levels of 13,744 mRNAs were altered on day 7 post-CFA, of which 49.67% were up-regulated and 50.33% were down-regulated. Specifically, 102 mRNAs (51 up and 51 down) were significantly regulated. Using quantitative real-time PCR, we verified the changes in differentially expressed lncRNAs in the injured DRG.

Conclusion

These results suggest that microarray-based RNA sequencing can be used to identify altered lncRNAs and relevant mRNAs in the DRG of rats with knee joint inflammation.

SUBMITTER: Bai Q

PROVIDER: S-EPMC7604464 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Publications

Transcriptome Analysis of Dorsal Root Ganglion in Rats with Knee Joint Inflammation.

Bai Qian Q Cao Jing J Dong Tieli T Tao Feng F

Journal of pain research 20201028

<h4>Background</h4>Rheumatoid arthritis (RA) leads to pain through alteration of gene expression. Although gene expression alteration in knee cartilage or peripheral blood from RA patients has been identified using microarray, it remains unclear whether long non-coding RNA (lncRNA)-mediated gene regulation occurs in primary sensory neurons of dorsal root ganglia (DRG) during RA-like joint inflammation. In the present study, we aimed to analyze lncRNA and related mRNA profiles in the DRG in a kne ...[more]

PMID: 33149663

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Project description:BackgroundPrimary and metastatic cancers that affect bone are frequently associated with severe and intractable pain. The mechanisms underlying the development of bone cancer pain are largely unknown. The aim of this study was to determine whether enhanced excitability of primary sensory neurons contributed to peripheral sensitization and tumor-induced hyperalgesia during cancer condition. In this study, using techniques of whole-cell patch-clamp recording associated with immunofluorescent staining, single-cell reverse-transcriptase PCR and behavioral test, we investigated whether the intrinsic membrane properties and the excitability of small-sized dorsal root ganglion (DRG) neurons altered in a rat model of bone cancer pain, and whether suppression of DRG neurons activity inhibited the bone cancer-induced pain.ResultsOur present study showed that implantation of MRMT-1 tumor cells into the tibial canal in rats produced significant mechanical and thermal hyperalgesia in the ipsilateral hind paw. Moreover, implantation of tumor cells provoked spontaneous discharges and tonic excitatory discharges evoked by a depolarizing current pulse in small-sized DRG neurons. In line with these findings, alterations in intrinsic membrane properties that reflect the enhanced neuronal excitability were observed in small DRG neurons in bone cancer rats, of which including: 1) depolarized resting membrane potential (RMP); 2) decreased input resistance (Rin); 3) a marked reduction in current threshold (CT) and voltage threshold (TP) of action potential (AP); 4) a dramatic decrease in amplitude, overshot, and duration of evoked action potentials as well as in amplitude and duration of afterhyperpolarization (AHP); and 5) a significant increase in the firing frequency of evoked action potentials. Here, the decreased AP threshold and increased firing frequency of evoked action potentials implicate the occurrence of hyperexcitability in small-sized DRG neurons in bone cancer rats. In addiotion, immunofluorescent staining and single-cell reverse-transcriptase PCR revealed that in isolated small DRG neurons, most neurons were IB4-positive, or expressed TRPV1 or CGRP, indicating that most recorded small DRG neurons were nociceptive neurons. Finally, using in vivo behavioral test, we found that blockade of DRG neurons activity by TTX inhibited the tumor-evoked mechanical allodynia and thermal hyperalgesia in bone cancer rats, implicating that the enhanced excitability of primary sensory neurons underlied the development of bone cancer pain.ConclusionsOur present results suggest that implantation of tumor cells into the tibial canal in rats induces an enhanced excitability of small-sized DRG neurons that is probably as results of alterations in intrinsic electrogenic properties of these neurons. Therefore, alterations in intrinsic membrane properties associated with the hyperexcitability of primary sensory neurons likely contribute to the peripheral sensitization and tumor-induced hyperalgesia under cancer condition.

Dataset Information

Transcriptome Analysis of Dorsal Root Ganglion in Rats with Knee Joint Inflammation.

Background

Methods

Results

Conclusion

Publications

Transcriptome Analysis of Dorsal Root Ganglion in Rats with Knee Joint Inflammation.

Similar Datasets

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