Evidence map›Paper›PMID 35858555›Full record

ArticleCell reports2022

In vitro atlas of dorsal spinal interneurons reveals Wnt signaling as a critical regulator of progenitor expansion.

Sandeep Gupta, Riki Kawaguchi, Eric Heinrichs, Salena Gallardo, Stephanie Castellanos, Igor Mandric, Bennett G Novitch, Samantha J Butler

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

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 22 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

8 authors at 1 institution in 1 country.

Sandeep GuptaDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: sandeepgupta@ucla.edu.
Riki KawaguchiDepartment of Psychiatry, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Eric HeinrichsDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Genetics and Genomics Graduate Program, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Salena GallardoDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Molecular Biology Interdepartmental Graduate Program, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Stephanie CastellanosDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA; CIRM Bridges to Research Program, California State University, Northridge, Los Angeles, CA, USA.
Igor MandricDepartment of Computer Science, Samueli School of Engineering, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Bennett G NovitchDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA; Intellectual & Developmental Disabilities Research Center, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Samantha J ButlerDepartment of Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA; Intellectual & Developmental Disabilities Research Center, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: butlersj@ucla.edu.
University of California, Los Angeles · US

Funding

UCLA IDDRC: Translational CoreP50HD103557 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SUSAN Y BOOKHEIMER · 2020 to 2026
$9.6M
Assessing the mechanisms directing cell fate in the dorsal spinal cordR01NS123187 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAMANTHA J BUTLER · 2022 to 2026
$2.2M
Diverse roles of the Bone Morphogenetic Proteins in the developing spinal cordR01NS085097 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BUTLER, SAMANTHA J · 2014 to 2018
$1.7M
Molecular Pathways Controlling Respiratory Motor Neuron Formation and FunctionR01NS085227 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI NOVITCH, BENNETT G · 2015 to 2019
$1.6M
Notch-mediated modulation of Sonic hedgehog signaling in neural fate specification and differentiationR21NS115012 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI NOVITCH, BENNETT G · 2020 to 2021
$424k
NINDS NIH HHS R01 NS085097NINDS NIH HHS R01 NS085227NINDS NIH HHS R01 NS123187NINDS NIH HHS R21 NS115012
6 · The paper itself

Abstract

Restoring sensation after injury or disease requires a reproducible method for generating large quantities of bona fide somatosensory interneurons. Toward this goal, we assess the mechanisms by which dorsal spinal interneurons (dIs; dI1-dI6) can be derived from mouse embryonic stem cells (mESCs). Using two developmentally relevant growth factors, retinoic acid (RA) and bone morphogenetic protein (BMP) 4, we recapitulate the complete in vivo program of dI differentiation through a neuromesodermal intermediate. Transcriptional profiling reveals that mESC-derived dIs strikingly resemble endogenous dIs, with the correct molecular and functional signatures. We further demonstrate that RA specifies dI4-dI6 fates through a default multipotential state, while the addition of BMP4 induces dI1-dI3 fates and activates Wnt signaling to enhance progenitor proliferation. Constitutively activating Wnt signaling permits the dramatic expansion of neural progenitor cultures. These cultures retain the capacity to differentiate into diverse populations of dIs, thereby providing a method of increasing neuronal yield.

Indexed as

Gene Expression Regulation, DevelopmentalWnt Signaling PathwayAnimalsCell DifferentiationInterneuronsMiceSpinal CordTretinoinTretinoinBMP signalingCP: Stem cell researchembryonic stem cellsexpansion culturespsychoactive drug signaturesretinoic acidsensory interneuronssingle-cell profilingspinal cordWnt signaling

Identifiers

PMID35858555
PMCPMC9414195
OpenAlexW4286250799

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.