Evidence map›Paper›PMID 40878823›Full record

ArticleOrthodontics & craniofacial research2025

Lats1/2 Differentially Modulate the Proliferative State of Dental Epithelial Progenitors and Ameloblasts in the Murine Incisor.

Zhiyue Zhang, Shilpa Upadhyay, Colleen Luong, Wei Du, Jimmy K Hu

Abstract read
In one paragraph

Article in Orthodontics & craniofacial research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Zhiyue ZhangSchool of Dentistry, University of California Los Angeles, Los Angeles, California, USA.
Shilpa UpadhyaySchool of Dentistry, University of California Los Angeles, Los Angeles, California, USA.
Colleen LuongSchool of Dentistry, University of California Los Angeles, Los Angeles, California, USA.
Wei DuState Key Laboratory of Oral Diseases and National Center for Stomatology and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
Jimmy K HuSchool of Dentistry, University of California Los Angeles, Los Angeles, California, USA.ORCID https://orcid.org/0000-0003-1035-0779

Funding

Mechanical regulation of transcription in dental epithelial stem cells through cell packing and tissue forcesR01DE030471 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Jimmy Kuang-Hsien Hu · 2022 to 2026
$1.8M
Using single cell transcriptomic analysis to uncover genetic pathways for de novo generation of dental epithelial progenitorsR03DE030205 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HU, JIMMY KUANG-HSIEN · 2021 to 2022
$312k
NIDCR NIH HHS R01 DE030471NIDCR NIH HHS R01DE030471NIDCR NIH HHS R03 DE030205NIDCR NIH HHS R03DE030205Sichuan Science and Technology Program 2025ZNSFSC1583West China Hospital of Stomatology, Sichuan University RCDWJS2023-11
6 · The paper itself

Abstract

OBJECTIVE(S): Yes-Associated Protein (YAP) is a critical regulator of cell proliferation and differentiation, having the capacity to convert differentiated cells into somatic stem cells in several contexts. Here we investigate the plasticity of adult mouse dental epithelial cells by testing the effects of ectopic YAP activation in dental epithelial progenitors and differentiated ameloblasts during incisor renewal. MATERIALS AND

methodsUsing mice with dental epithelial deletion of Lats1 and Lats2, which encode negative regulators of YAP, we assessed how ectopic YAP activation altered tissue structure, cell proliferation, and differentiation via histological analysis, EdU/BrdU labeling, and immunostaining. We also treated primary dental epithelial cells in 3D culture with TRULI, a LATS inhibitor, to test cell plasticity outside the context of an intact tissue.

resultsYAP overactivation in the incisor epithelium induced ectopic cell proliferation in the apical bud and prolonged the proliferative state of dental epithelial progenitors, leading to a thickened suprabasal layer. However, ameloblasts remained non-proliferative. Tissue structures and differentiation of pre-ameloblasts were disrupted. Finally, LATS inhibition was able to induce colony formation in some dissociated, 3D-cultured ameloblasts.

conclusionYAP activation promotes the expansion of dental epithelial progenitors but not ameloblasts in vivo, suggesting irreversible differentiation during tooth renewal. However, when dissociated, some ameloblasts acquire plasticity. This offers a strategy to manipulate proliferation in dental epithelial cells under different conditions and may have broader applications in orthodontics, where a modular control of progenitors and differentiated cells is critical for ensuring safe stem cell-based treatments.

Indexed as

Adaptor Proteins, Signal TransducingAmeloblastsCell ProliferationEpithelial CellsIncisorProtein Serine-Threonine KinasesStem CellsTumor Suppressor ProteinsAnimalsCell DifferentiationMiceYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingLats1 protein, mouseLATS2 protein, mouseProtein Serine-Threonine KinasesTumor Suppressor ProteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID40878823
PMCPMC12690751

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.