Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 17 min ago
Peer-reviewedCC BY-NCAllergy, asthma & immunology research

Cadherin-26 Promotes Airway Remodeling via Stabilizing Epithelial Expression of the Epidermal Growth Factor Receptor in Asthma.

  • Jiali Gao1,2,3
  • Gongqi Chen1,2,4
  • Chunli Huang1,2
  • Zhen Wang1,2
  • Wei Gu1,2
  • Huiru Jie1,2
  • Tiantian Xiong1,2
  • Yuchen Feng1,2
  • Lingling Yi1,2
  • Dan Cheng5
  • Guohua Zhen1,6
6 affiliations
  1. 1Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  2. 2Key Laboratory of Respiratory Diseases, National Health Commission of the People's Republic of China, and National Clinical Research Center for Respiratory Diseases, Wuhan, China.
  3. 3Department of Respiratory and Critical Care Medicine, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, China.
  4. 4Department of General Practice, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  5. 5Department of Respiratory and Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, China. [email protected].
  6. 6Key Laboratory of Respiratory Diseases, National Health Commission of the People's Republic of China, and National Clinical Research Center for Respiratory Diseases, Wuhan, China. [email protected].
Read full textPDFDOICite

Abstract

Purpose

Activation of epidermal growth factor receptor (EGFR) signaling in airway epithelial cells leads to epithelial-mesenchymal transformation (EMT) and airway remodeling in asthma. However, the mechanism regulating EGFR expression is not fully understood. We hypothesized that cadherin-26 (CDH26), a highly expressed cadherin in airway epithelium, promotes airway remodeling via regulating EGFR signaling in asthma.Methods

The expression of CDH26 in airway brush cells of asthmatic patients was examined using quantitative polymerase chain reaction. Airway hyperresponsiveness and remodeling were assessed in the house dust mite (HDM)-sensitized and -challenged Cdh26-deficient mice. The role and mechanism of CDH26 in epidermal growth factor (EGF)-induced EMT were measured in cultured human bronchial epithelial BEAS-2B cells.Results

The expression of CDH26 in airway brush cells was significantly correlated with the thickness of airway basement membrane in asthma patients. Cdh26 deficiency significantly reduced airway hyperresponsiveness and remodeling in HDM-sensitized and -challenged mouse model. In cultured human bronchial epithelial BEAS-2B cells, CDH26 knockdown inhibited EGF-induced EMT, whereas overexpression of CDH26 promoted EGF-induced EMT. Furthermore, CDH26 knockdown suppressed EGF-induced activation of EGFR signaling including phosphatidylinositol 3-kinase and AKT phosphorylation. By contrast, CDH26 overexpression intensified EGF-induced activation of EGFR signaling. Mechanistically, CDH26 knockdown promoted the proteasomal degradation of the EGFR.Conclusions

CDH26 promoted airway remodeling via stabilizing the epithelial expression of EGFR and sustaining the activation of EGFR signaling in asthma. Thus, CDH26 can be a potential therapeutic target for airway remodeling in asthma.

Related

  1. UCHL1 Promotes Epithelial–Mesenchymal Transition Through E-Cadherin and N-Cadherin Switch in Endometrial Cancer
    Azusa Kobayashi, Kohshiro Nakao, Naoki Inoue +5
    BiomedicinesPeer-reviewedCC BYFull textGeneral medicineEurope PMC
  2. The atypical cadherin CELSR2 regulates distinct epithelial-mesenchymal states and oxidative phosphorylation in triple-negative breast cancer
    J. Koren, N.-I. Y. Saidani, A. El kaoutari +13
    bioRxivPreprintAll rights reservedFull textOncologybioRxiv
  3. P-cadherin Overexpression Induces Partial Epithelial-to-Mesenchymal Transition and Confers Chemoresistance in Dysplastic Oral Epithelial Cells.
    Aaron Suresh Mody, Christine Paulette Neal, Kristen Kim Drinkwater +2
    Journal of CancerPeer-reviewedCC BYFull textOncologyEurope PMC
  4. Vascular endothelial cadherin remodeling is associated with endothelial barrier dysfunction in chronic subdural hematoma
    K. Ravina, M. C. Renton, J. Darden +3
    bioRxivPreprintCC BY-NC-NDFull textNeurologybioRxiv
  5. Naringenin Enhances the Inhibitory Effect of Regorafenib on HepG2 Hepatocellular Carcinoma Cell Viability with Modulation of E-Cadherin and MRP1 Gene Expression
    Sara A. Gaballah, Ahmed I. Abulsoud, Asmaa Saleh +1
    International Journal of Molecular SciencesPeer-reviewedCC BY 4.0Full textPharmacology & toxicologyCrossrefEurope PMC

Cite

BibTeXRIS
BibTeX
@article{gao2026cadherin26,
  title = {{Cadherin-26 Promotes Airway Remodeling via Stabilizing Epithelial Expression of the Epidermal Growth Factor Receptor in Asthma.}},
  author = {Jiali Gao and Gongqi Chen and Chunli Huang and Zhen Wang and Wei Gu and Huiru Jie and Tiantian Xiong and Yuchen Feng and Lingling Yi and Dan Cheng and Guohua Zhen},
  journal = {Allergy, asthma \& immunology research},
  year = {2026},
  month = sep,
  doi = {10.4168/aair.2026.18.5.702},
  url = {https://europepmc.org/article/MED/42845226},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Cadherin-26 Promotes Airway Remodeling via Stabilizing Epithelial Expression of the Epidermal Growth Factor Receptor in Asthma.
AU  - Jiali Gao
AU  - Gongqi Chen
AU  - Chunli Huang
AU  - Zhen Wang
AU  - Wei Gu
AU  - Huiru Jie
AU  - Tiantian Xiong
AU  - Yuchen Feng
AU  - Lingling Yi
AU  - Dan Cheng
AU  - Guohua Zhen
PY  - 2026
DA  - 2026/09/01
JO  - Allergy, asthma & immunology research
DO  - 10.4168/aair.2026.18.5.702
UR  - https://europepmc.org/article/MED/42845226
AB  - Purpose  Activation of epidermal growth factor receptor (EGFR) signaling in airway epithelial cells leads to epithelial-mesenchymal transformation (EMT) and airway remodeling in asthma. However, the mechanism regulating EGFR expression is not fully understood. We hypothesized that cadherin-26 (CDH26), a highly expressed cadherin in airway epithelium, promotes airway remodeling via regulating EGFR signaling in asthma.Methods  The expression of CDH26 in airway brush cells of asthmatic patients was examined using quantitative polymerase chain reaction. Airway hyperresponsiveness and remodeling were assessed in the house dust mite (HDM)-sensitized and -challenged Cdh26-deficient mice. The role and mechanism of CDH26 in epidermal growth factor (EGF)-induced EMT were measured in cultured human bronchial epithelial BEAS-2B cells.Results  The expression of CDH26 in airway brush cells was significantly correlated with the thickness of airway basement membrane in asthma patients. Cdh26 deficiency significantly reduced airway hyperresponsiveness and remodeling in HDM-sensitized and -challenged mouse model. In cultured human bronchial epithelial BEAS-2B cells, CDH26 knockdown inhibited EGF-induced EMT, whereas overexpression of CDH26 promoted EGF-induced EMT. Furthermore, CDH26 knockdown suppressed EGF-induced activation of EGFR signaling including phosphatidylinositol 3-kinase and AKT phosphorylation. By contrast, CDH26 overexpression intensified EGF-induced activation of EGFR signaling. Mechanistically, CDH26 knockdown promoted the proteasomal degradation of the EGFR.Conclusions  CDH26 promoted airway remodeling via stabilizing the epithelial expression of EGFR and sustaining the activation of EGFR signaling in asthma. Thus, CDH26 can be a potential therapeutic target for airway remodeling in asthma.
SN  - 2092-7355
SN  - 2092-7363
ER  -