Evidence map›Paper›PMID 27485117›Full record

ArticleMolecular brain2016

Astrocyte-secreted thrombospondin-1 modulates synapse and spine defects in the fragile X mouse model.

Connie Cheng, Sally K M Lau, Laurie C Doering

Open access · goldAbstract read
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 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 82 citations in OpenAlex.

  1. Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026
    Review
  2. The tyrosine phosphatase STEP is a developmental suppressor of synaptogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. Astrocyte Regulation of Synapse Formation, Maturation, and Elimination.Cold Spring Harbor perspectives in biology · 2024
    Review
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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

3 authors at 1 institution in 1 country.

Connie ChengMcMaster Integrative Neuroscience Discovery and Study Program (MINDS), McMaster University, 1280 Main Street West, Hamilton, Ontario, L8S 4L8, Canada.
Sally K M LauDepartment of Pathology and Molecular Medicine, McMaster University, 1200 Main Street West, HSC 1R15A, Hamilton, Ontario, L8N 3Z5, Canada.
Laurie C DoeringMcMaster Integrative Neuroscience Discovery and Study Program (MINDS), McMaster University, 1280 Main Street West, Hamilton, Ontario, L8S 4L8, Canada. doering@mcmaster.ca.
McMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes are key participants in various aspects of brain development and function, many of which are executed via secreted proteins. Defects in astrocyte signaling are implicated in neurodevelopmental disorders characterized by abnormal neural circuitry such as Fragile X syndrome (FXS). In animal models of FXS, the loss in expression of the Fragile X mental retardation 1 protein (FMRP) from astrocytes is associated with delayed dendrite maturation and improper synapse formation; however, the effect of astrocyte-derived factors on the development of neurons is not known. Thrombospondin-1 (TSP-1) is an important astrocyte-secreted protein that is involved in the regulation of spine development and synaptogenesis. In this study, we found that cultured astrocytes isolated from an Fmr1 knockout (Fmr1 KO) mouse model of FXS displayed a significant decrease in TSP-1 protein expression compared to the wildtype (WT) astrocytes. Correspondingly, Fmr1 KO hippocampal neurons exhibited morphological deficits in dendritic spines and alterations in excitatory synapse formation following long-term culture. All spine and synaptic abnormalities were prevented in the presence of either astrocyte-conditioned media or a feeder layer derived from FMRP-expressing astrocytes, or following the application of exogenous TSP-1. Importantly, this work demonstrates the integral role of astrocyte-secreted signals in the establishment of neuronal communication and identifies soluble TSP-1 as a potential therapeutic target for Fragile X syndrome.

Indexed as

AnimalsAstrocytesCulture Media, ConditionedDendritesDisease Models, AnimalFeeder CellsFemaleFragile X SyndromeHippocampusMaleMice, KnockoutSpineSynapsesThrombospondin 1Culture Media, ConditionedThrombospondin 1AstrocytesAutismDendritic spinesFragile X syndromeSecreted factorSynapsesThrombospondin-1

Identifiers

PMID27485117
PMCPMC4971702
OpenAlexW2479769265

What Socratic 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 Socratic graph.