Evidence map›Paper›PMID 35394873›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

Monocyte-derived SDF1 supports optic nerve regeneration and alters retinal ganglion cells' response to Pten deletion.

Lili Xie, Ling-Ping Cen, Yiqing Li, Hui-Ya Gilbert, Oleksandr Strelko, Cynthia Berlinicke, Mihaela A Stavarache, Madeline Ma, Yongting Wang, Qi Cui and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  12. The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025
    Review
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  14. Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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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

14 authors at 4 institutions in 3 countries.

Lili XieDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-5157-1482
Ling-Ping CenDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0003-3876-0606
Yiqing LiDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-3483-7189
Hui-Ya GilbertDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-3170-388X
Oleksandr StrelkoDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0001-7876-1887
Cynthia BerlinickeDepartment of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
Mihaela A StavaracheLaboratory of Molecular Neurosurgery, Department of Neurological Surgery, Weill Cornell Medical College, New York, NY 10065.ORCID 0000-0002-8120-7470
Madeline MaDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.
Yongting WangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200240, China.ORCID 0000-0002-5841-6557
Qi CuiDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.
Michael G KaplittLaboratory of Molecular Neurosurgery, Department of Neurological Surgery, Weill Cornell Medical College, New York, NY 10065.ORCID 0000-0002-8979-2459
Donald J ZackDepartment of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287.ORCID 0000-0002-7966-1973
Larry I BenowitzDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-0277-7222
Yuqin YinDepartment of Neurosurgery, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-0980-6954
Boston Children's Hospital · USCornell University · USJohns Hopkins University · USShanghai Jiao Tong University · CN

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Genetic Analysis and Manipulation Core (GAEC)P50HD105351 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SCOTT Loren POMEROY, MUSTAFA SAHIN · 2021 to 2026
$9.4M
MOLECULAR BASES OF NEURONAL CONNECTIVITYR01EY005690 · NEI · MC LEAN HOSPITAL (BELMONT, MA) · PI BENOWITZ, LARRY IRA · 1985 to 2012
$4.7M
Dual Leucine Zipper Kinase (DLK) as a Mediator of Retinal Ganglion Cell InjuryR01EY023754 · NEI · JOHNS HOPKINS UNIVERSITY · PI ZACK, DONALD J. · 2013 to 2016
$1.6M
HHS | NIH | National Eye Institute (NEI) R01EY05690NEI NIH HHS R01 EY005690NEI NIH HHS R01 EY023754NICHD NIH HHS P30 HD018655NICHD NIH HHS P50 HD105351
6 · The paper itself

Abstract

Although mammalian retinal ganglion cells (RGCs) normally cannot regenerate axons nor survive after optic nerve injury, this failure is partially reversed by inducing sterile inflammation in the eye. Infiltrative myeloid cells express the axogenic protein oncomodulin (Ocm) but additional, as-yet-unidentified, factors are also required. We show here that infiltrative macrophages express stromal cell–derived factor 1 (SDF1, CXCL12), which plays a central role in this regard. Among many growth factors tested in culture, only SDF1 enhances Ocm activity, an effect mediated through intracellular cyclic AMP (cAMP) elevation and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) activation. SDF1 deficiency in myeloid cells (CXCL12flx/flxLysM-Cre−/+ mice) or deletion of the SDF1 receptor CXCR4 in RGCs (intraocular AAV2-Cre in CXCR4flx/flx mice) or SDF1 antagonist AMD3100 greatly suppresses inflammation-induced regeneration and decreases RGC survival to baseline levels. Conversely, SDF1 induces optic nerve regeneration and RGC survival, and, when combined with Ocm/cAMP, SDF1 increases axon regeneration to levels similar to those induced by intraocular inflammation. In contrast to deletion of phosphatase and tensin homolog (Pten), which promotes regeneration selectively from αRGCs, SDF1 promotes regeneration from non-αRGCs and enables the latter cells to respond robustly to Pten deletion; however, SDF1 surprisingly diminishes the response of αRGCs to Pten deletion. When combined with inflammation and Pten deletion, SDF1 enables many RGCs to regenerate axons the entire length of the optic nerve. Thus, SDF1 complements the effects of Ocm in mediating inflammation-induced regeneration and enables different RGC subtypes to respond to Pten deletion.

Indexed as

Optic Nerve InjuriesRetinal Ganglion CellsAxonsChemokine CXCL12MonocytesNerve RegenerationPTEN PhosphohydrolaseChemokine CXCL12PTEN Phosphohydrolaseinflammationmacrophagesoptic nerve regenerationRGC subtypesSDF1

Identifiers

PMID35394873
PMCPMC9169637
OpenAlexW4223491796

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.