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Hsa-miR-34a mediated repression of corticotrophin releasing hormone receptor 1 regulates pro-opiomelanocortin expression in patients with complex regional pain syndrome
Journal article   Open access   Peer reviewed

Hsa-miR-34a mediated repression of corticotrophin releasing hormone receptor 1 regulates pro-opiomelanocortin expression in patients with complex regional pain syndrome

Botros B Shenoda, Guillermo M Alexander and Seena K Ajit
Journal of translational medicine, v 14(1), pp 64-64
03 Mar 2016
PMID: 26940669
url
https://doi.org/10.1186/s12967-016-0820-1View
Published, Version of Record (VoR) Open

Abstract

Body Mass Index Reproducibility of Results Receptors, Corticotropin-Releasing Hormone - metabolism Jurkat Cells Humans Gene Expression Regulation Receptors, Corticotropin-Releasing Hormone - genetics MicroRNAs - metabolism Complex Regional Pain Syndromes - blood Pro-Opiomelanocortin - blood Pro-Opiomelanocortin - metabolism alpha-MSH - blood HEK293 Cells Ketamine - therapeutic use MicroRNAs - genetics Complex Regional Pain Syndromes - drug therapy Adrenocorticotropic Hormone - blood Complex Regional Pain Syndromes - genetics beta-Endorphin - blood
Ketamine provides relief for a subset of patients with complex regional pain syndrome (CRPS). The poor responders had a lower body mass index (BMI) relative to responders. Regulation of proopiomelanocortin (POMC) expression is crucial in normal body weight homeostasis. The main objectives of this study were to investigate the mechanisms underlying lower BMI characterizing CRPS patients responding poorly to intravenous ketamine therapy and identify potential biomarkers for predicting response. We investigated POMC transcript levels in blood from CRPS patients grouped as responders and poor responders to ketamine therapy. Plasma levels of β-endorphin, ACTH and α-MSH were measured by ELISA. We previously identified differential expression of small noncoding microRNA hsa-miR-34a in blood between responders and poor responders. We investigated whether a 11-fold downregulation of hsa-miR-34a in poor responders relative to responders is contributing to the differences in POMC levels by targeting POMC regulator CRHR1. Binding of miR-34a to CRHR1 was assessed using reporter assay; changes in mRNA and protein levels of CRHR1 were used to determine the regulation of CRHR1 by miR-34a. RNA from blood of CRPS and control subjects were used for quantitative PCR for CRHR1. Though ketamine treatment did not alter POMC expression, poor responders had higher levels of POMC mRNA than responders, both before and after treatment. Corticotropin-releasing hormone (CRH) is a key regulator of POMC expression and the biological effects are mediated through its receptor corticotrophin releasing hormone receptor 1 (CRHR1). We show that hsa-miR-34a is a negative regulator of CRHR1; overexpression of hsa-miR-34a in Jurkat cells resulted in reduction of CRH-mediated POMC expression. Poor responders had higher expression of CRHR1 transcripts than responders, indicating a regulatory role for miR-34a. In addition, we found positive correlations between the pretreatment levels of miR-34a to BMI and response to ketamine therapy. Our findings indicate a mechanism by which hsa-miR-34a can regulate the CRH/CRHR1/POMC axis and may influence BMI. Studies in larger patient cohorts are required to confirm the biomarker utility of circulating hsa-miR-34a levels in predicting treatment response to ketamine therapy.

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Web of Science research areas
Medicine, Research & Experimental
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