Single-nucleus RNA sequencing of the cells obtained from acupoint BL23 (Shenshu) in low back pain.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE312510 | GEO | 2025/12/31
REPOSITORIES: GEO
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| GSE312510_RAW.tar | Raw | |||
| filelist.txt | Txt |
Items per page: 5 1 - 3 of 3 |
Similar Datasets
Project description:Fine needle stimulation also known as acupuncture is a traditional Chinese medical practice which causes relief of pain. We demonstrated that it caused neovascularization and enhanced recovery of blood perfusion in a ischemic portion of skeletal muscle in rats with hindlimb ischemia. Therefore we evaluated the effect of fine needle stimulation on skeletal muscle at gene expression level Keywords: Evaluation of physical stimulation
2007-09-01 | GSE8911 | GEO
Project description:Fine needle stimulation also known as acupuncture is a traditional Chinese medical practice which causes relief of pain. We demonstrated that it caused neovascularization and enhanced recovery of blood perfusion in a ischemic portion of skeletal muscle in rats with hindlimb ischemia. Therefore we evaluated the effect of fine needle stimulation on skeletal muscle at gene expression level Experiment Overall Design: With 0.14mm diameter stainless steel needle, a hundred pricks were applied in a 100 square mili-meter region on addductor portion of the left rat hindlimb. Right hindlimb was left intact as control. 24 hrs after fine needle stimulation, skeletal muscle sample was resected from adductor muscle of fine needle stimulated left hindlimb and non-stimulated right hindlimbs, respectively. Then gene expression analysis with microarray was conducted on each skelatal muscle sample.
2008-06-16 | E-GEOD-8911 | biostudies-arrayexpress
Project description:Objective To investigate the mechanism of action of "Biaoben acupoint " acupuncture in treating Lumbar Disc Herniation (LDH) by identifying differentially expressed plasma proteins (DEPs) using timsTOF Pro-based 4D Data-Independent Acquisition (DIA) proteomics and correlating them with clinical indicators. Methods This study enrolled 10 healthy subjects (healthy group) and 10 patients with LDH (experimental group). The experimental group received "Biaoben acupoint" acupuncture treatment for 3 weeks. Clinical outcomes, including Visual Analogue Scale (VAS) for pain, Oswestry Disability Index (ODI) for lumbar function, and Japanese Orthopaedic Association (JOA) score for neurological status, were assessed before and after treatment. Plasma samples were collected for proteomic analysis. Results Acupuncture treatment significantly improved VAS, ODI, and JOA scores in the experimental group compared to baseline (p<0.001). Proteomic analysis quantified 3685 proteins, identifying 376 DEPs across the healthy group and the experimental group (before and after treatment). Bioinformatics analysis revealed that these DEPs were primarily enriched in pathways related to cell structure and adhesion (e.g., cytoskeleton remodeling, focal adhesion), inflammation and immune signaling (e.g., chemokine and cytokine signaling), and cell signal transduction (e.g., calcium signaling, Rap1 pathway). Core DEPs included ACTB, CXCR4, ACTN1, CXCL12, SELP, and CCN2. Correlation analysis demonstrated that the expression levels of CXCL12, ACTN1, CXCR4, and CCN2 were significantly correlated with VAS, ODI, and JOA scores. Conclusion "Biaoben acupoint" acupuncture likely exerts its therapeutic effects by modulating multiple biological pathways related to inflammatory/immune responses, cytoskeleton organization, cell structure/adhesion, and tissue repair, thereby improving pain, lumbar function, and neurological deficits in LDH patients. Proteins such as CXCL12, ACTN1, CXCR4, and CCN2 are potential key mediators of these therapeutic effects.
| PXD067489 |
Project description:Purpose: We used RNA sequencing to investigate the effect of acupuncture treatment on retinal transcritome after optic nerve injury Methods: Retinal mRNA profiles of 5-week-old wild-type (WT), optic nerve crush injury (ONC), ONC injury with acupuncture treatment at acupoint GB20 (ONC-F) and ONC injury with acupuncture treatment at acupoint BL1 (ONC-J) mice were generated by deep sequencing, in triplicate, using Illumina Hiseq platform. The sequence reads that passed quality filters were analyzed with DESeq2 R package to identify differently expressed genes with padj<0.05. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: RNA-seq revealed that 436 genes including 31 transcription factors (TFs) were changed after injury, which include many well-known neural degeneration related TFs such as Jun, Ddit3, Atf3 and Atf4. Interestingly, acupuncture treatment at acupoint GB20 (Fengchi) or BL1(Jingming) after ONC injury both resulted in change of retinal gene expression, compared with ONC injury without treatment; furthermore, acupuncture treatment also reversed several gene expression status induced by axon injury. Conclusions: Our research first reported that acupuncture treatment after injury can regulated retinal transcriptome and reversed the gene expression level induced after injury, which will provide novel therapeutic targets for treatment of retinopathy diseases.
2019-11-12 | GSE131486 | GEO
Project description:Acupuncture treatment is based on acupoint stimulation; however, the biological basis is not understood. We stimulated one acupoint with catgut embedding (CEP) for 8 weeks and then used isobaric tags for relative and absolute quantitation to screen proteins with altered expression in adjacent acupoints of Sprague Dawley rats. The expression levels of 10 proteins, including kininogen (KNG), consistently changed >1.5-fold in all three acupoints in CEP versus sham CEP-treated rats. Eight-week, but not 3-day, CEP treatment enhanced KNG expression. The enhanced KNG expression among small vessels in the subcutaneous layer was revealed via immunofluorescence. Nitric oxide synthesis was enhanced similar to KNG. These findings uncover biological changes at acupoints and suggest the critical role of the KNG–nitric oxide signaling pathway in acupoint activation.
2022-02-16 | PXD024018 | Pride
Project description:Background. Inter- and intra-individual fluctuations in pain intensity pose a major challenge to treatment efficacy, with a majority perceiving their pain relief as inadequate. Recent preclinical studies have identified circadian rhythmicity as a potential contributor to these fluctuations and therapeutic target. Methods. We therefore sought to determine the impact of these rhythms in people with chronic low back pain (CLBP) through a detailed characterization, including questionnaires to evaluate biopsychosocial characteristics, ecological momentary assessment (7-day e-diaries at 8:00/14:00/20:00) to assess pain fluctuations, and intra-day blood transcriptomics (8:00/20:00) to identify genes/pathways of interest. Results. While most individuals displayed constant or variable/mixed pain phenotypes, a distinct subset had daily fluctuations of increasing pain scores (>30% change in intensity over 12-hours in ≥4/7 days). This population had no opioid users, better biopsychosocial profiles, and differentially expressed transcripts relative to other pain phenotypes. The circadian-governed neutrophil degranulation pathway was particularly enriched among arhythmic individuals; the link between neutrophil degranulation and opioid use was further confirmed in a separate CLBP cohort. Conclusion. Our findings identify pain rhythmicity and the circadian expression of neutrophil degranulation pathways as indicators of CLBP outcomes, which may help provide a personalized approach to phenotyping biopsychosocial characteristics and medication use. This highlights the need to better understand the impact of circadian rhythmicity across chronic pain conditions.
2025-07-16 | GSE295758 | GEO
Project description:We report the application of Affymetrix technology for high-throughput profiling of the transcriptome of the rheumatoid arthritis (RA) rat model induced by collagen type II (CIA), with acupuncture and Methotrexate+acupuncture treatment, as well as epidermal needle manipulation on healthy rat model.
2016-12-23 | GSE58456 | GEO
Project description:Purpose:Acupuncture exerts cardioprotective effect on myocardial I/R injury. In order to elucidate the potential mechanisms, RNA-seq by next generation sequencing was used to identify the rat genome-wide alterations by EA at Neiguan acupoint pretreatment in this study Methods: Adult male Sprague Dawley rats (250-300g) were divided into four groups: Sham operation(SO), I/R, electro-acupuncture at Neiguan pretreatment (EA) and electro-acupuncture at non-acupoint (NA) groups and myocardium mRNA profiles of rats in each group were generated by deep sequencing,using Illumina Hiseq 2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 20~43 million sequence reads per sample to the mouse genome (UCSC RN4) and identified 26190 22895 25160 22852 transcripts in the SO, I/R, EA and NA rats with TopHat and Cufflinks workflow respectively. Approximately 32% and 22% of the transcripts showed differential expression between the SO and I/R, I/R and EA , I/R and NA, respectively with a |log2 fold change |≥1. Conclusions: Our results for the first time generated genome-wide gene expression profiles both in the rat I/R model and in acupuncture treatment by high throughput sequencing. The optimized data analysis workflows reported here should provide a framework for acupuncture investigations of expression profiles.
2016-03-20 | GSE61840 | GEO
Project description:For over a millennium, mind-body interactions have fascinated scientists and doctors for their abilities to shape human perceptions of the external world 1,2. Placebo effects are striking demonstrations of mind-body interactions in which, in the absence of any treatment, a positive expectation of pain relief can reduce or even abolish the experience of pain 3–6. However, despite widespread recognition of the strength of placebo effects and their impact on everyday human experience and clinical trials for new analgesics, the neural circuit basis of the placebo effect has remained a mystery. Here, we show that analgesia from the expectation of pain relief is mediated by a distinct population of rostral anterior cingulate cortex (rACC) neurons that project to the pontine nuclei (rACC→Pn), a pair of brainstem pre-cerebellar nuclei with no established function in pain processing. To do this, we created a behavioral assay that models placebo analgesia by conditioning mice to expect pain relief when moving from a chamber with a heated floor to a second chamber. In this assay, an expectation of pain relief induces an analgesic effect that, like placebo analgesia in humans, is mediated by endogenous opioids. Calcium imaging of neural activity in freely moving mice and electrophysiological studies in cingulate cortical brain slices showed that expectations of pain relief boost the activity of rACC→Pn neurons and potentiate neurotransmission in this pathway. Transcriptomic studies of Pn neurons revealed an unusual abundance of opioid receptors in these cells, further suggesting a role in pain modulation. Selective inhibition of either the rACC→Pn pathway or of opioid-receptor-expressing Pn neurons disrupted placebo analgesia and decreased pain thresholds. Finally, a subset of cerebellar Purkinje cells exhibits activity patterns resembling those of rACC→Pn neurons during pain relief expectation, providing cellular-level evidence of a role for the cerebellum in cognitive pain modulation. Altogether, these findings elucidate longstanding mysteries surrounding the placebo effect by identifying a specific neural pathway that mediates expectation-based pain relief. This discovery opens the possibility of targeting this novel pathway with drugs or neurostimulation methods to treat pain. More broadly, our studies provide a framework for investigating the neural circuit basis of other mind-body interactions beyond those involving pain, and point to prefrontocortical-cerebellar communication as a potential basis for such effects.
2024-09-12 | GSE267264 | GEO
Project description:For over a millennium, mind-body interactions have fascinated scientists and doctors for their abilities to shape human perceptions of the external world 1,2. Placebo effects are striking demonstrations of mind-body interactions in which, in the absence of any treatment, a positive expectation of pain relief can reduce or even abolish the experience of pain 3–6. However, despite widespread recognition of the strength of placebo effects and their impact on everyday human experience and clinical trials for new analgesics, the neural circuit basis of the placebo effect has remained a mystery. Here, we show that analgesia from the expectation of pain relief is mediated by a distinct population of rostral anterior cingulate cortex (rACC) neurons that project to the pontine nuclei (rACC→Pn), a pair of brainstem pre-cerebellar nuclei with no established function in pain processing. To do this, we created a behavioral assay that models placebo analgesia by conditioning mice to expect pain relief when moving from a chamber with a heated floor to a second chamber. In this assay, an expectation of pain relief induces an analgesic effect that, like placebo analgesia in humans, is mediated by endogenous opioids. Calcium imaging of neural activity in freely moving mice and electrophysiological studies in cingulate cortical brain slices showed that expectations of pain relief boost the activity of rACC→Pn neurons and potentiate neurotransmission in this pathway. Transcriptomic studies of Pn neurons revealed an unusual abundance of opioid receptors in these cells, further suggesting a role in pain modulation. Selective inhibition of either the rACC→Pn pathway or of opioid-receptor-expressing Pn neurons disrupted placebo analgesia and decreased pain thresholds. Finally, a subset of cerebellar Purkinje cells exhibits activity patterns resembling those of rACC→Pn neurons during pain relief expectation, providing cellular-level evidence of a role for the cerebellum in cognitive pain modulation. Altogether, these findings elucidate longstanding mysteries surrounding the placebo effect by identifying a specific neural pathway that mediates expectation-based pain relief. This discovery opens the possibility of targeting this novel pathway with drugs or neurostimulation methods to treat pain. More broadly, our studies provide a framework for investigating the neural circuit basis of other mind-body interactions beyond those involving pain, and point to prefrontocortical-cerebellar communication as a potential basis for such effects.
2024-09-12 | GSE267265 | GEO