ArticleJournal of cellular and molecular medicine2020
MiR-101 promotes pain hypersensitivity in rats with chronic constriction injury via the MKP-1 mediated MAPK pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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
13 citing papers in PubMed, 26 citations in OpenAlex.
- Propofol attenuates pain hypersensitivity and neuroinflammation in chronic constriction injury rats by regulating miR-1249-3p/VEGFA axis.The Korean journal of pain · 2026Article
- Neuropathic Pain: Mapping the miRNA Landscape.Non-coding RNA · 2026Review
- miR-197, miR-101, and miR-143 and Pro-Inflammatory Cytokines in Migraine.Journal of clinical medicine · 2025Article
- Role of ncRNAs in the Development of Chronic Pain.Non-coding RNA · 2025Review
- The Role of miRNAs in Neuropathic Pain.Biomedicines · 2023Review
- CEBPα/miR-101b-3p promotes meningoencephalitis in mice infected with Angiostrongylus cantonensis by promoting microglial pyroptosis.Cell communication and signaling : CCS · 2023Article
- Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Distribution and possible function of galanin about headache and immune system in the rat dura mater.Scientific reports · 2022Article
- Electroacupuncture Suppresses CCI-Induced Neuropathic Pain through GABAA Receptors.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Mediators of Neuropathic Pain; Focus on Spinal Microglia, CSF-1, BDNF, CCL21, TNF-α, Wnt Ligands, and Interleukin 1β.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- microRNA-Based Network and Pathway Analysis for Neuropathic Pain in Rodent Models.Frontiers in molecular biosciences · 2021Article
- Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.Molecular medicine (Cambridge, Mass.) · 2020Article
- MiR-101 promotes pain hypersensitivity in rats with chronic constriction injury via the MKP-1 mediated MAPK pathway.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was performed to characterize the effect of microRNA-101 (miR-101) on the pain hypersensitivity in CCI rat models with the involvement of mitogen-activated protein kinase phosphatase 1 (MKP-1) in spinal cord microglial cells. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) in the developed CCI models were determined to assess the hypersensitivity of rats to mechanical stimulation and thermal pain. To assess inflammation, the levels of interleukin (IL)-1β, IL-6 and tumour necrosis factor-α (TNF-α) in the spinal dorsal horns of CCI rats and lipopolysaccharide (LPS)-activated microglial cells were examined. miR-101 and MKP-1 gain- and loss-of-function experiments were conducted in in vivo and in vitro settings to examine the roles of miR-101 and MKP-1 in CCI hypersensitivity and inflammation. The results showed that miR-101 was highly expressed in the spinal dorsal horn and microglial cells of CCI rat models. Furthermore, overexpression of miR-101 promoted the pain hypersensitivity in CCI rat models by reducing MWT and TWL. The overexpression of miR-101 also promoted inflammation in LPS-exposed microglial cells, as indicated by increased levels of IL-1β, IL-6 and TNF-α. MiR-101 was shown to target MKP-1, inhibiting its expression. Moreover, miR-101 promoted pain hypersensitivity in CCI rat models by inhibiting MKP-1 expression and activating the mitogen-activated protein kinase (MAPK) signalling pathway. Taken together, miR-101 could potentially promote hypersensitivity and inflammatory response of microglial cells and aggravate neuropathic pain in CCI rat models by inhibiting MKP-1 in the MAPK signalling pathway.
Indexed as
Identifiers
What Socratic 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 Socratic graph.