ArticlePloS one2011
Profile of microRNAs following rat sciatic nerve injury by deep sequencing: implication for mechanisms of nerve regeneration.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- How miRNAs Regulate Schwann Cells during Peripheral Nerve Regeneration-A Systemic Review.International journal of molecular sciences · 2022Pooled it
- Biosynthesis inhibition of miR-142-5p in a NCellular & molecular biology letters · 2025Article
- Nanomedicine and voltage-gated sodium channel blockers in pain management: a game changer or a lost cause?Drug delivery and translational research · 2024Review
- MicroRNA-9 promotes axon regeneration of mauthner-cell in zebrafish via her6/ calcium activity pathway.Cellular and molecular life sciences : CMLS · 2024Article
- Predictive and concurrent validity of pain sensitivity phenotype, neuropeptidomics and neuroepigenetics in the MI-RAT osteoarthritic surgical model in rats.Frontiers in cell and developmental biology · 2024Article
- Regulation of Schwann cell proliferation and migration via miR-195-5p-induced Crebl2 downregulation upon peripheral nerve damage.Frontiers in cellular neuroscience · 2023Article
- Dysregulated miR-29a-3p/PMP22 Modulates Schwann Cell Proliferation and Migration During Peripheral Nerve Regeneration.Molecular neurobiology · 2022Article
- DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain.International journal of molecular sciences · 2022Review
- miR-140-3p suppresses the proliferation and migration of macrophages.Genetics and molecular biology · 2022Article
- Transcriptome analysis of molecular mechanisms underlying facial nerve injury repair in rats.Neural regeneration research · 2021Article
- miR-328a-3p stimulates endothelial cell migration and tubulogenesis.Experimental and therapeutic medicine · 2021Article
- Transcriptomic analysis reveals essential microRNAs after peripheral nerve injury.Neural regeneration research · 2021Article
- Changes of pro-inflammatory and anti-inflammatory macrophages after peripheral nerve injury.RSC advances · 2020Article
- Protein phosphorylation profiling of peripheral nerve regeneration after autologous nerve grafting.Molecular and cellular biochemistry · 2020Article
- Intra-axonal mechanisms driving axon regeneration.Brain research · 2020Review
- Temporal changes in the spinal cord transcriptome after peripheral nerve injury.Neural regeneration research · 2020Article
- Genetic changes in rat proximal nerve stumps after sciatic nerve transection.Annals of translational medicine · 2019Article
- Let-7d modulates the proliferation, migration, tubulogenesis of endothelial cells.Molecular and cellular biochemistry · 2019Article
- Novel miRNA, miR-sc14, promotes Schwann cell proliferation and migration.Neural regeneration research · 2019Article
- Inhibition of MicroRNA-195 Alleviates Neuropathic Pain by Targeting Patched1 and Inhibiting SHH Signaling Pathway Activation.Neurochemical research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unlike the central nervous system, peripheral nerves can regenerate when damaged. MicroRNA (miRNA) is a novel class of small, non-coding RNA that regulates gene expression at the post-transcriptional level. Here, we report regular alterations of miRNA expression following rat sciatic nerve injury using deep sequencing. We harvested dorsal root ganglia tissues and the proximal stumps of the nerve, and identified 201 and 225 known miRNAs with significant expression variance at five time points in these tissues after sciatic nerve transaction, respectively. Subsequently, hierarchical clustering, miRNA expression pattern and co-expression network were performed. We screened out specific miRNAs and further obtained the intersection genes through target analysis software (Targetscan and miRanda). Moreover, GO and KEGG enrichment analyses of these intersection genes were performed. The bioinformatics analysis indicated that the potential targets for these miRNAs were involved in nerve regeneration, including neurogenesis, neuron differentiation, vesicle-mediated transport, homophilic cell adhesion and negative regulation of programmed cell death that were known to play important roles in regulating nerve repair. Finally, we combined differentially expressed mRNA with the predicted targets for selecting inverse miRNA-target pairs. Our results show that the abnormal expression of miRNA may contribute to illustrate the molecular mechanisms of nerve regeneration and that miRNAs are potential targets for therapeutic interventions and may enhance intrinsic regenerative ability.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.