The limited role of RGS10 on NFκB and cytokine transcript levels in peritoneal macrophages under the influence of opioid analgesics
5 affiliations
- 1Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, Florida, United States of America
- 2Department of Neuroscience, College of Medicine, University of Florida, Gainesville, Florida, United States of America
- 3McKnight Brain Institute, University of Florida, Gainesville, Florida, United States of America
- 4Department of Neurology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America
- 5Stark Neuroscience Research Institute, Indianapolis, Indiana, United States of America
Abstract
Regulator of G-protein signaling 10 (RGS10) has been shown to regulate multiple inflammatory pathways relevant to disease pathogenesis. Of particular importance is the ability of RGS10 to negatively regulate the NFkB pathway, a prominent pro-inflammatory pathway implicated in multiple inflammatory disease phenotypes. However, the exact mechanism by which RGS10 regulates NFκB is unknown. Given that RGS10 translocates to the nucleus upon stimulation, we hypothesize that RGS10 may regulate NFκB at the transcript level. To determine whether RGS10 influences NFκB transcript levels, we stimulated peritoneal macrophages from RGS10 Knockout (KO) and B6 mice and collected cell lysate and conditioned media over a 24-hour period to assess transcript levels of NFκB and related pro-inflammatory cytokines as well as secreted cytokine levels. Here we found a limited and transient influence of RGS10 on transcript levels of NFκB subunits and NFκB-dependent cytokines. However, RGS10 displayed a more robust negative regulation of secreted protein levels of certain pro-inflammatory cytokines. Importantly, this study required the use of opioid analgesics prior to the collection of peritoneal macrophages and therefore reflects the role of RGS10 on pro-inflammatory transcript and protein levels when opioid analgesics are present. Overall, this study indicates that RGS10 may not serve as an important transcriptional regulator of NFκB related cytokine production under the influence of opioid analgesics. Further studies are warranted to understand the influence of opioid analgesics on RGS10 function and the mechanism by which RGS10 regulates NFκB activity.
Related
- Nociceptin/Orphanin FQ Peptide (NOP) Receptor Agonists as Novel Analgesics in Pain Medicine
- Terminus est: Repurposing public RNA-seq data to map 3′ transcript termini in bacteria
- The role of the fruitless P3 transcript in development in Drosophila melanogaster
- Why rescue-based transcript ranking can mislead: normalization displacement and shared-control coupling in perturbation transcriptomics
- SpliceCOV: Supervised Filtering of RNA-Seq-Derived Transcript Features Improves Transcriptome Assembly
BibTeX
@article{posey2026limited,
title = {{The limited role of RGS10 on NFκB and cytokine transcript levels in peritoneal macrophages under the influence of opioid analgesics}},
author = {Janna E. Jernigan Posey and Kruthika Dheeravath and Cassandra L. Cole and Noelle K. Neighbarger and Kelly B. Menees and Malú Gámez Tansey},
journal = {PLOS One},
year = {2026},
month = sep,
doi = {10.1371/journal.pone.0343480},
url = {https://doi.org/10.1371/journal.pone.0343480},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The limited role of RGS10 on NFκB and cytokine transcript levels in peritoneal macrophages under the influence of opioid analgesics
AU - Janna E. Jernigan Posey
AU - Kruthika Dheeravath
AU - Cassandra L. Cole
AU - Noelle K. Neighbarger
AU - Kelly B. Menees
AU - Malú Gámez Tansey
PY - 2026
DA - 2026/09/23
JO - PLOS One
DO - 10.1371/journal.pone.0343480
UR - https://doi.org/10.1371/journal.pone.0343480
AB - Regulator of G-protein signaling 10 (RGS10) has been shown to regulate multiple inflammatory pathways relevant to disease pathogenesis. Of particular importance is the ability of RGS10 to negatively regulate the NFkB pathway, a prominent pro-inflammatory pathway implicated in multiple inflammatory disease phenotypes. However, the exact mechanism by which RGS10 regulates NFκB is unknown. Given that RGS10 translocates to the nucleus upon stimulation, we hypothesize that RGS10 may regulate NFκB at the transcript level. To determine whether RGS10 influences NFκB transcript levels, we stimulated peritoneal macrophages from RGS10 Knockout (KO) and B6 mice and collected cell lysate and conditioned media over a 24-hour period to assess transcript levels of NFκB and related pro-inflammatory cytokines as well as secreted cytokine levels. Here we found a limited and transient influence of RGS10 on transcript levels of NFκB subunits and NFκB-dependent cytokines. However, RGS10 displayed a more robust negative regulation of secreted protein levels of certain pro-inflammatory cytokines. Importantly, this study required the use of opioid analgesics prior to the collection of peritoneal macrophages and therefore reflects the role of RGS10 on pro-inflammatory transcript and protein levels when opioid analgesics are present. Overall, this study indicates that RGS10 may not serve as an important transcriptional regulator of NFκB related cytokine production under the influence of opioid analgesics. Further studies are warranted to understand the influence of opioid analgesics on RGS10 function and the mechanism by which RGS10 regulates NFκB activity.
SN - 1932-6203
ER -