Evidence map›Paper›PMID 37219951›Full record

ArticleJCI insight2023

TIAM1 acts as an actin organization regulator to control adipose tissue-derived pericyte cell fate.

Ginny Ching-Yun Hsu, Yiyun Wang, Amy Z Lu, Mario A Gomez-Salazar, Jiajia Xu, Dongqing Li, Carolyn Meyers, Stefano Negri, Sintawat Wangsiricharoen, Kristen Broderick and 3 more

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

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
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  4. 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

13 authors at 2 institutions in 2 countries.

Ginny Ching-Yun HsuDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Yiyun WangDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Amy Z LuDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Mario A Gomez-SalazarDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Jiajia XuDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Dongqing LiDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Carolyn MeyersDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Stefano NegriDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Sintawat WangsiricharoenDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Kristen BroderickDepartment of Plastic Surgery, Johns Hopkins University, Baltimore, Maryland, USA.
Bruno PeaultUCLA and Orthopaedic Hospital Department of Orthopaedic Surgery and Orthopaedic Hospital Research Center, Los Angeles, California, USA.
Carol MorrisDepartment of Orthopaedic Surgery, Johns Hopkins University, Baltimore, Maryland, USA.
Aaron W JamesDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.
Johns Hopkins University · USOrthopaedic Hospital · US

Funding

NELL-1 Systemic Therapy for OsteoporosisR01AR066782 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI EASLEY, JEREMIAH, TING, KANG · 2014 to 2018
$2.0M
Direct and indirect contributions of perivascular stem cells to bone healingR01AR070773 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI JAMES, AARON W · 2017 to 2021
$1.4M
TIAM1 dictates lineage commitment in skeletal and soft tissue pericytesK08DE031347 · NIDCR · OREGON HEALTH & SCIENCE UNIVERSITY · PI Ginny Ching-Yun Hsu · 2022 to 2026
$830k
NELL-1 isoforms for the systemic treatment of osteoporosisK08AR068316 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JAMES, AARON W · 2015 to 2019
$534k
NIAMS NIH HHS K08 AR068316NIAMS NIH HHS R01 AR066782NIAMS NIH HHS R01 AR070773NIDCR NIH HHS K08 DE031347
6 · The paper itself

Abstract

Pericytes are multipotent mesenchymal precursor cells that demonstrate tissue-specific properties. In this study, by comparing human adipose tissue- and periosteum-derived pericyte microarrays, we identified T cell lymphoma invasion and metastasis 1 (TIAM1) as a key regulator of cell morphology and differentiation decisions. TIAM1 represented a tissue-specific determinant between predispositions for adipocytic versus osteoblastic differentiation in human adipose tissue-derived pericytes. TIAM1 overexpression promoted an adipogenic phenotype, whereas its downregulation amplified osteogenic differentiation. These results were replicated in vivo, in which TIAM1 misexpression altered bone or adipose tissue generation in an intramuscular xenograft animal model. Changes in pericyte differentiation potential induced by TIAM1 misexpression correlated with actin organization and altered cytoskeletal morphology. Small molecule inhibitors of either small GTPase Rac1 or RhoA/ROCK signaling reversed TIAM1-induced morphology and differentiation in pericytes. In summary, our results demonstrate that TIAM1 regulates the cellular morphology and differentiation potential of human pericytes, representing a molecular switch between osteogenic and adipogenic cell fates.

Indexed as

ActinsPericytesAdipose TissueAnimalsCell DifferentiationGuanine Nucleotide Exchange FactorsHumansOsteogenesisT-Lymphoma Invasion and Metastasis-inducing Protein 1ActinsGuanine Nucleotide Exchange FactorsTIAM1 protein, humanT-Lymphoma Invasion and Metastasis-inducing Protein 1Adipose tissueBone BiologyBone diseaseCell BiologyPericytes

Identifiers

PMID37219951
PMCPMC10371340
OpenAlexW4377565056

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.