Evidence map›Paper›PMID 32150531›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

Protective effect of BMSCs-derived exosomes mediated by BDNF on TBI via miR-216a-5p.

Huiyou Xu, Zhilong Jia, Ke Ma, Jian Zhang, Chen Dai, Zitong Yao, Wusheng Deng, Jianzhong Su, Renjie Wang, Xuyi Chen

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Huiyou XuDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Zhilong JiaDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Ke MaDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Jian ZhangDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Chen DaiDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Zitong YaoDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Wusheng DengDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Jianzhong SuDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Renjie WangDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Xuyi ChenDepartment of Neurosurgery, Characteristic Medical Center of Chinese People's Armed Police Force; Institution of Brain Trauma and Neurology Disease of People's Armed Police Forces; Tianjin Key Laboratory of Neurotrauma Repair, Tianjin, China (mainland).
Chinese People's Armed Police ForceChinese People's Armed Police General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Transplantation of exosomes derived from mesenchymal stem cells (MSCs-Exo) can improve the recovery of neurological function in rats after traumatic brain injury (TBI). We tested a new hypothesis that BDNF-mediated MSCs-Exo could effectively promote functional recovery and neurogenesis of rats after TBI. MATERIAL AND METHOD BMSCs of rats were extracted by whole bone marrow culture, BDNF was added to BMSCs for intervention, supernatant was collected, and exosomes were separated and purified by hypercentrifugation. Exosomes were identified by WB, TEM and particle size analysis and subsequently used in cell and animal experiments. We investigated the recovery of sensorimotor function and spatial learning ability, inflammation inhibition and neuron regeneration in rats after TBI. RESULTS Compared with group MSCs-Exo, group BDNF-mediated MSCs-Exo showed better effects in promoting the recovery of sensorimotor function and spatial learning ability. BDNF-mediated MSCs-Exo successfully inhibited inflammation and promoted neuronal regeneration in vivo and in vitro. We further analyzed miRNA in BDNF-mediated MSCs-Exo and MSCs-Exo, and found that the expression of miR-216a-5p in BDNF-mediated MSCs-Exo was significantly higher than that in MSCs-Exo by qRT-PCR. Rescue experiment indicated that miR-216a-5p has a similar function to BDNF-mediated MSCs-Exo. CONCLUSIONS In conclusion, we found that BDNF-mediated MSCs-Exo can better promote neurogenesis and inhibit apoptosis than MSCs-Exo in rats after TBI, and the mechanism may be related to the high expression of miR-216a-5p.

Indexed as

AnimalsApoptosisBrainBrain-Derived Neurotrophic FactorBrain Injuries, TraumaticCell Line, TumorCell MovementCulture MediaDisease Models, AnimalExosomesHumansMaleMesenchymal Stem CellsMicroRNAsNerve RegenerationNeurogenesisBdnf protein, ratBrain-Derived Neurotrophic FactorCulture MediaMicroRNAsMIRN216 microRNA, rat

Identifiers

PMID32150531
PMCPMC7081927
OpenAlexW3002444274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.