Evidence map›Paper›PMID 38898476›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Wnt5a-mediated autophagy contributes to the epithelial-mesenchymal transition of human bronchial epithelial cells during asthma.

Yu-Biao Liu, Xiao-Hua Tan, Hui-Hui Yang, Jin-Tong Yang, Chen-Yu Zhang, Ling Jin, Nan-Shi-Yu Yang, Cha-Xiang Guan, Yong Zhou, Shao-Kun Liu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Review
  6. 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.

Yu-Biao LiuDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Xiao-Hua TanExperimental Center of Medical Morphology, School of Basic Medicine Science, Central South University, Changsha, Hunan, 410078, China.
Hui-Hui YangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, China.
Jin-Tong YangKey Laboratory of General University of Hunan Province, Basic and Clinic Research in Major Respiratory Disease, Changsha, Hunan, 410078, China.
Chen-Yu ZhangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, China.
Ling JinDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, China.
Nan-Shi-Yu YangDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, China.
Cha-Xiang GuanDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, China.
Yong ZhouDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha, Hunan, 410078, China.
Shao-Kun LiuDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. shaokunliu228@csu.edu.cn.
Jian-Bing XiongDepartment of Emergency, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China. xiongjb@csu.edu.cn.ORCID 0009-0003-6517-9013

Funding

Health Commission of Hunan Province 202202014633Health Commission of Hunan Province B202303028704Health Commission of Hunan Province D202302019023Natural Science Foundation of Hunan Province 2019JJ40453
6 · The paper itself

Abstract

backgroundThe epithelial-mesenchymal transition (EMT) of human bronchial epithelial cells (HBECs) is essential for airway remodeling during asthma. Wnt5a has been implicated in various lung diseases, while its role in the EMT of HBECs during asthma is yet to be determined. This study sought to define whether Wnt5a initiated EMT, leading to airway remodeling through the induction of autophagy in HBECs.

methodsMicroarray analysis was used to investigate the expression change of WNT5A in asthma patients. In parallel, EMT models were induced using 16HBE cells by exposing them to house dust mites (HDM) or interleukin-4 (IL-4), and then the expression of Wnt5a was observed. Using in vitro gain- and loss-of-function approaches via Wnt5a mimic peptide FOXY5 and Wnt5a inhibitor BOX5, the alterations in the expression of the epithelial marker E-cadherin and the mesenchymal marker protein were observed. Mechanistically, the Ca

resultsAsthma patients exhibited a significant increase in the gene expression of WNT5A compared to the healthy control. Upon HDM and IL-4 treatments, we observed that Wnt5a gene and protein expression levels were significantly increased in 16HBE cells. Interestingly, Wnt5a mimic peptide FOXY5 significantly inhibited E-cadherin and upregulated α-SMA, Collagen I, and autophagy marker proteins (Beclin1 and LC3-II). Rhodamine-phalloidin staining showed that FOXY5 resulted in a rearrangement of the cytoskeleton and an increase in the quantity of stress fibers in 16HBE cells. Importantly, blocking Wnt5a with BOX5 significantly inhibited autophagy and EMT induced by IL-4 in 16HBE cells. Mechanistically, autophagy inhibitor 3-MA and CaMKII inhibitor KN-93 reduced the EMT of 16HBE cells caused by FOXY5, as well as the increase in stress fibers, cell adhesion, and autophagy.

conclusionThis study illustrates a new link in the Wnt5a-Ca

Indexed as

AsthmaAutophagyEpithelial CellsEpithelial-Mesenchymal TransitionWnt-5a ProteinAdultBronchiCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell LineFemaleHumansMaleMiddle AgedSignal TransductionCalcium-Calmodulin-Dependent Protein Kinase Type 2Wnt-5a ProteinWNT5A protein, humanAirway remodelingAsthmaAutophagyCalmodulin-dependent kinase IIEpithelial-mesenchymal transitionWnt5a

Identifiers

PMID38898476
PMCPMC11188189

What Socratic holds

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LicenceCC BY
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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.