ArticleJournal of translational medicine2016
Hsa-miR-34a mediated repression of corticotrophin releasing hormone receptor 1 regulates pro-opiomelanocortin expression in patients with complex regional pain syndrome.
Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Plasma-Derived Small Extracellular Vesicles miR- 182 - 5p Is a Potential Biomarker for Diagnosing Major Depressive Disorder.Molecular neurobiology · 2025Article
- LncRNA XIST: A Breakthrough in Inflammation-related Diseases.Current medicinal chemistry · 2025Review
- Communicating pain: emerging axonal signaling in peripheral neuropathic pain.Frontiers in neuroanatomy · 2024Review
- CpG Methylation Levels in HPA Axis Genes Predict Chronic Pain Outcomes Following Trauma Exposure.The journal of pain · 2023Article
- Hsa-miR-605 regulates the proinflammatory chemokine CXCL5 in complex regional pain syndrome.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Article
- Pre-reproductive stress in adolescent female rats alters oocyte microRNA expression and offspring phenotypes: pharmacological interventions and putative mechanisms.Translational psychiatry · 2021Article
- Computational Functional Genomics-Based AmpliSeq™ Panel for Next-Generation Sequencing of Key Genes of Pain.International journal of molecular sciences · 2021Article
- Non-coding RNAs in neuropathic pain.Neuronal signaling · 2020Review
- Exosome microRNA signatures in patients with complex regional pain syndrome undergoing plasma exchange.Journal of translational medicine · 2019Article
- Somatostatin receptor subtype 5 modifies hypothalamic-pituitary-adrenal axis stress function.JCI insight · 2018Article
- Complex regional pain syndrome - phenotypic characteristics and potential biomarkers.Nature reviews. Neurology · 2018Review
- miR-34a-mediated regulation of XIST in female cells under inflammation.Journal of pain research · 2018Article
- Overview of microRNA Modulation in Analgesic Research.Current protocols in pharmacology · 2017Review
- Article
- The role of miR-190a-5p contributes to diabetic neuropathic pain via targeting SLC17A6.Journal of pain research · 2017Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKetamine 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.
methodsWe 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.
resultsThough 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.
conclusionsOur 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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