Evidence map›Paper›PMID 39428818›Full record

ArticleDisease models & mechanisms2024

Hippo cooperates with p53 to regulate lung airway mucous cell metaplasia.

Jiangying Liu, Dan Luo, Haidi Huang, Rongzi Mu, Jianghong Yuan, Ming Jiang, Chuwen Lin, Honggang Xiang, Xinhua Lin, Haihan Song and 1 more

Abstract read
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In one paragraph

Article in Disease models & mechanisms, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Jiangying LiuState Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic and Developmental Sciences, Inner Mongolia Research Institute, Shenzhen Research Institute, Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.
Dan LuoState Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic and Developmental Sciences, Inner Mongolia Research Institute, Shenzhen Research Institute, Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.
Haidi HuangState Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic and Developmental Sciences, Inner Mongolia Research Institute, Shenzhen Research Institute, Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.
Rongzi MuState Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic and Developmental Sciences, Inner Mongolia Research Institute, Shenzhen Research Institute, Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.
Jianghong YuanState Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic and Developmental Sciences, Inner Mongolia Research Institute, Shenzhen Research Institute, Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.
Ming JiangCenter for Genetic Medicine, The Fourth Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310030, Zhejiang, China.
Chuwen LinDepartment of Histology and Embryology, School of Medicine, Shenzhen Campus of Sun Yat-Sen University, Shenzhen 518107, Guangdong, China.
Honggang XiangDepartment of General Surgery, Pudong New Area People's Hospital, Shanghai 201299, China.
Xinhua LinState Key Laboratory of Genetic Engineering, School of Life Sciences, Greater Bay Area Institute of Precision Medicine (Guangzhou), Zhongshan Hospital, Fudan University Shanghai, Shanghai 200438, China.
Haihan SongCentral Lab, Shanghai Key Laboratory of Pathogenic Fungi Medical Testing, Shanghai Pudong New Area People's Hospital, Shanghai 201299, China.
Yongchun ZhangState Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic and Developmental Sciences, Inner Mongolia Research Institute, Shenzhen Research Institute, Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China.ORCID 0009-0009-9949-0604

Funding

Medicine-Engineering Interdisciplinary Research Fund of Shanghai Jiao Tong University YG2023QNB31National Key Research and Development Program of China 2022YFA0912600National Natural Science Foundation of China 32170831Natural Science Foundation of Inner Mongolia Autonomous Region 2024MS03003Natural Science Foundation of Shanghai 22ZR1435300Natural Science Foundation of Shanghai Municipality 22ZR1435300Science and Technology Planning Project of Shenzen Municipality JCYJ20230807110800002Shanghai Jiao Tong University YG2023QNB31Shenzhen Science and Technology Innovation Committee JCYJ20230807110800002
6 · The paper itself

Abstract

Airway mucous cell metaplasia is a significant feature of many chronic airway diseases, such as chronic obstructive pulmonary disease, cystic fibrosis and asthma. However, the mechanisms underlying this process remain poorly understood. Here, we employed in vivo mouse genetic models to demonstrate that Hippo and p53 (encoded by Trp53) cooperate to modulate the differentiation of club cells into goblet cells. We revealed that ablation of Mst1 (Stk4) and Mst2 (Stk3), encoding the core components of Hippo signaling, significantly reduces mucous metaplasia in the lung airways in a lipopolysaccharide (LPS)-induced lung inflammation murine model while promoting club cell proliferation in a Yap (Yap1)-dependent manner. Additionally, we showed that deleting Mst1/2 is sufficient to suppress p53 deficiency-mediated goblet cell metaplasia. Finally, single-cell RNA-sequencing analysis revealed downregulation of YAP and p53 signaling in goblet cells in human airways. These findings underscore the important role of Hippo and p53 signaling in regulating airway mucous metaplasia.

Indexed as

Goblet CellsHippo Signaling PathwayLungMetaplasiaProtein Serine-Threonine KinasesTumor Suppressor Protein p53YAP-Signaling ProteinsAdaptor Proteins, Signal TransducingAnimalsCell DifferentiationCell ProliferationHippo KinasesHumansMiceMice, Inbred C57BLRespiratory MucosaAdaptor Proteins, Signal TransducingHippo KinasesProtein Serine-Threonine KinasesSerine-Threonine Kinase 3Stk3 protein, mouseStk4 protein, mouseTumor Suppressor Protein p53Yap1 protein, mouseYAP-Signaling ProteinsClub cellGoblet cellHippo signalingMucous cell metaplasiap53

Identifiers

PMID39428818
PMCPMC11603118

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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.