Evidence map›Paper›PMID 27153974›Full record

ArticleMolecular brain2016

Rescuing macrophage normal function in spinal cord injury with embryonic stem cell conditioned media.

Lei Guo, Alyssa J Rolfe, Xi Wang, Wenjiao Tai, Zhijian Cheng, Kai Cao, Xiaoming Chen, Yunsheng Xu, Dongming Sun, Jinhua Li and 4 more

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

Article in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. New Diagnostic and Therapeutic Targets for Spinal Cord Injury: GRN Gene.Journal of cellular and molecular medicine · 2025
    Article
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  10. Review
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  18. Article
  19. Mesenchymal Stem Cell-Macrophage Choreography Supporting Spinal Cord Repair.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018
    Review
  20. Article
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

14 authors at 7 institutions in 3 countries.

Lei GuoDepartment of Orthopedics, The Second Affiliated Hospital of Xian Jiaotong University, Xian, 710004, China.
Alyssa J RolfeDepartment of Biomedical Sciences, Florida State University, College of Medicine, 1115 West Street, Tallahassee, FL, 32306, USA.
Xi WangW. M. Keck Center for Collaborative Neuroscience, Rutgers, The State University of New Jersey, New Brunswick, NJ, 08854, USA.
Wenjiao TaiDepartment of Biomedical Sciences, Florida State University, College of Medicine, 1115 West Street, Tallahassee, FL, 32306, USA.
Zhijian ChengDepartment of Orthopedics, The Second Affiliated Hospital of Xian Jiaotong University, Xian, 710004, China.
Kai CaoDepartment of Orthopedics, The Second Affiliated Hospital of Xian Jiaotong University, Xian, 710004, China.
Xiaoming ChenInstitute of Inflammation and Diseases, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Yunsheng XuInstitute of Inflammation and Diseases, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Dongming SunW. M. Keck Center for Collaborative Neuroscience, Rutgers, The State University of New Jersey, New Brunswick, NJ, 08854, USA.
Jinhua LiDepartment of Anatomy and Developmental Biology, Monash University, Clayton, VIC, 3800, Australia.
Xijing HeDepartment of Orthopedics, The Second Affiliated Hospital of Xian Jiaotong University, Xian, 710004, China.
Wise YoungW. M. Keck Center for Collaborative Neuroscience, Rutgers, The State University of New Jersey, New Brunswick, NJ, 08854, USA.
Jianqing FanStatistical Laboratory, Princeton University, Princeton, NJ, 08540, USA.
Yi RenDepartment of Biomedical Sciences, Florida State University, College of Medicine, 1115 West Street, Tallahassee, FL, 32306, USA. yi.ren@med.fsu.edu.
Florida State University · USRutgers, The State University of New Jersey · USSecond Affiliated Hospital of Xi'an Jiaotong University · CNFirst Affiliated Hospital of Wenzhou Medical University · CNMonash University · AUPrinceton University · USWenzhou Medical University · CN

Funding

Statistical Methods for Ultrahigh-dimensional Biomedical DataR01GM072611 · NIGMS · PRINCETON UNIVERSITY · PI CATTANEO, MATIAS DAMIAN · 2006 to 2021
$4.2M
Quantitative Methods for Genome-wide Analysis of Macrophage Activation by ESCsR01GM100474 · NIGMS · PRINCETON UNIVERSITY · PI FAN, JIANQING · 2011 to 2014
$1.5M
NIGMS NIH HHS R01 GM072611NIGMS NIH HHS R01 GM100474
6 · The paper itself

Abstract

backgroundMacrophages play an important role in the inflammatory responses involved with spinal cord injury (SCI). We have previously demonstrated that infiltrated bone marrow-derived macrophages (BMDMs) engulf myelin debris, forming myelin-laden macrophages (mye-Mϕ). These mye-Mϕ promote disease progression through their pro-inflammatory phenotype, enhanced neurotoxicity, and impaired phagocytic capacity for apoptotic cells. We thus hypothesize that the excessive accumulation of mye-Mϕ is the root of secondary injury, and that targeting mye-Mϕ represents an efficient strategy to improve the local inflammatory microenvironment in injured spinal cords and to further motor neuron function recovery. In this study, we administer murine embryonic stem cell conditioned media (ESC-M) as a cell-free stem cell based therapy to treat a mouse model of SCI.

resultsWe showed that BMDMs, but not microglial cells, engulf myelin debris generated at the injury site. Phagocytosis of myelin debris leads to the formation of mye-Mϕ in the injured spinal cord, which are surrounded by activated microglia cells. These mye-Mϕ are pro-inflammatory and lose the normal macrophage phagocytic capacity for apoptotic cells. We therefore focus on how to trigger lipid efflux from mye-Mϕ and thus restore their function. Using ESC-M as an immune modulating treatment for inflammatory damage after SCI, we rescued mye-Mϕ function and improved functional locomotor recovery. ESC-M treatment on mye-Mϕ resulted in improved exocytosis of internalized lipids and a normal capacity for apoptotic cell phagocytosis. Furthermore, when ESC-M was administered intraperitoneally after SCI, animals exhibited significant improvements in locomotor recovery. Examination of spinal cords of the ESC-M treated mice revealed similar improvements in macrophage function as well as a shift towards a more anti-inflammatory environment at the lesion and parenchyma.

conclusionsThe embryonic stem cell conditioned media can be used as an effective treatment for SCI to resolve inflammation and improve functional recovery while circumventing the complications involved in whole cell transplantation.

Indexed as

AnimalsApoptosisBone Marrow CellsCulture Media, ConditionedFoam CellsInflammationLipidsMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMouse Embryonic Stem CellsMyelin SheathNeutrophilsPhagocytosisRecovery of FunctionCulture Media, ConditionedLipidsBone Marrow-Derived Macrophages (BMDMs)Embryonic Stem Cells (ESCs)InflammationMicrogliaMyelinSpinal Cord Injury (SCI)

Identifiers

PMID27153974
PMCPMC4858887
OpenAlexW2345811531

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.