Increased epithelial galectin‐13 expression associates with eosinophilic airway inflammation in asthma

Yi, Lingling; Zhang, Shuchen; Feng, Yuchen; Wu, Wenliang; Chang, Chenli; Chen, Dian; Chen, Shengchong; Zhao, Jianping; Zhen, Guohua

doi:10.1111/cea.13961

Cited by 10 publications

(11 citation statements)

References 37 publications

(73 reference statements)

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“…In addition to pulmonary function parameters, PTPRH protein level in sputum supernatant was not only positively correlated with IL-4, IL-5, IL-13, which were associated with Th2 high asthma, but also associated with SERPINB2 and POSTN, Th2 signature. 22,23 Our study found that treatment with PTPRH relieved HDM challenge-induced airway inflammation and mucus overproduction in asthma model. Inflammation leading to an overproduction of mucus induces airflow obstruction.…”

Section: Discussionmentioning

confidence: 69%

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PTPRH Alleviates Airway Obstruction and Th2 Inflammation in Asthma as a Protective Factor

Chen¹,

Li²,

Zeng³

et al. 2022

JAA

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Purpose: PTPRH inhibits EGFR activity directly in cancer patients and activated EGFR induces goblet cell hyperplasia and mucus hypersecretion in asthma. However, the function of PTPRH in asthma remains unknown. The purpose of this study was to access the association of PTPRH with asthma and its underlying mechanism. Patients and Methods:We examined the PTPRH level in asthma patients (n = 108) and healthy controls (n = 35), and analyzed the correlations between PTPRH and asthma-related indicators. Human bronchial epithelial cell (HBECs) transfected with PTPRH and asthma mouse model were set up to investigate the function of PTPRH. Results: The expression of PTPRH was significantly increased and correlated with pulmonary function parameters, including airway obstruction, and T-helper2 (Th2) associated markers in asthma patients. PTPRH increased in the house dust mite (HDM)-induced asthmatic mice, while Th2 airway inflammation and Muc5ac suppressed when treated with PTPRH. Accordingly, PTPRH expression was markedly increased in IL-13-stimulated HBECs but PTPRH over-expression suppressed MUC5AC. Moreover, HBECs transfected with over-expressed PTPRH inhibited the phosphorylation of EGFR, ERK1/2 and AKT, while induced against PTPRH in HBECs dephosphorylated of EGFR, ERK1/2 and AKT. Conclusion: PTPRH reduces MUC5AC secretion to alleviate airway obstruction in asthma via potential phosphorylating of EGFR/ ERK1/2/AKT signaling pathway, which may provide possible therapeutic implications for asthma.

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Section: Discussionmentioning

confidence: 69%

“…SERPINB2 and POSTN, is an epithelial gene signature for Th2 high asthma. 22,23 These data indicates that PTPRH involves in asthma featured with Th2 inflammation.…”

Section: Ptprh Protein Levels Were Associated With Th2 High Asthmamentioning

confidence: 74%

PTPRH Alleviates Airway Obstruction and Th2 Inflammation in Asthma as a Protective Factor

Chen¹,

Li²,

Zeng³

et al. 2022

JAA

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“…18 Another study showed that Gal-13, a novel marker of airway eosinophilia in asthma, could lead to increased inflammatory infiltration and apoptosis of allergic airway eosinophils by upregulating MCP-1 and eotaxin-1 expression. 19 In this study, we found that Gal-7 was upregulated in TGF-β1-induced BEAS-2B cells, and was regulated by the upstream transcription factor CTCF to accelerate cell damage. The above findings further clarify the possible regulatory mechanism of Gal-7 in the process of asthma.…”

Section: Ctcf Activated the Jnk/stat3 Axis Through Transcriptional Re...mentioning

confidence: 65%

“…Tian et al found increased bronchial epithelial detachment and apoptosis, airway smooth muscle, and basement membrane thickening in Gal‐7 transgenic (+) mice when treated with respiratory syncytial virus or ovalbumin 18 . Another study showed that Gal‐13, a novel marker of airway eosinophilia in asthma, could lead to increased inflammatory infiltration and apoptosis of allergic airway eosinophils by upregulating MCP‐1 and eotaxin‐1 expression 19 . In this study, we found that Gal‐7 was upregulated in TGF‐β1‐induced BEAS‐2B cells, and was regulated by the upstream transcription factor CTCF to accelerate cell damage.…”

Section: Discussionmentioning

confidence: 99%

CCCTC‐binding factor transcriptionally regulates Galectin‐7 and activates the JNK/STAT3 axis to aggravate bronchial epithelial cell injury

Sun

Shen

et al. 2021

Pediatric Pulmonology

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Objective Studies have shown that the expression of CCCTC‐binding factor (CTCF) is significantly upregulated in the airway epithelial cells of asthmatic patients, suggesting that CTCF may play an important role in the progression of asthma. Material/Methods Human bronchial epithelial cells BEAS‐2B were stimulated with transforming growth factor‐β1 (TGF‐β1) at a concentration of 10 ng/ml, and CTCF overexpression plasmid and CTCF small interfering RNA were transfected into the cells. The proliferation, apoptosis, inflammatory factor secretion, and airway remodeling marker protein expression of injured cells were detected. We bidirectionally regulated Galectin‐7 expression in TGF‐β1‐induced BEAS‐2B cells and overexpress CTCF, while interfering with Galectin‐7 to further explore the regulatory effect of CTCF on Galectin‐7. We introduced SP600125, a c‐Jun N‐terminal kinase c‐Jun (JNK) pathway inhibitor, to investigate whether CTCF affects asthma progression through the JNK pathway. Results The expression of CTCF in BEAS‐2B cells induced by TGF‐β1 was significantly upregulated, interfering with CTCF expression promoted cell proliferation, inhibited apoptosis, reduced inflammatory factors secretion, and decreased the expression of airway remodeling marker protein. Luciferase reporter gene analysis and chromatin immunoprecipitation verified that CTCF directly bound to Galectin‐7 promoter. The effect of Galectin‐7 on cells is consistent with the effect of CTCF on cells. The regulatory effect of CTCF on injured cells was indeed mediated by activation of the JNK/STAT3 axis. Conclusions CTCF transcriptionally regulated Galectin‐7 and activated JNK/STAT3 axis to aggravate bronchial epithelial cell injury.

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“…With the exception of HBB , SERPINB11 , and DPP4 , the trend of other candidate DEGs was consistent between the above two datasets. Candidate DEGs including SERPINB2 , POSTN , and CLCA1 have already been reported to participate in asthma ( 22 ). Among the remaining candidate DEGs, the expressions of two members of the SPRRs family ( SPRR1B and SPRR3 ) were upregulated ( Figures 1B–E ).…”

Section: Resultsmentioning

confidence: 99%

Small Proline-Rich Protein 3 Regulates IL-33/ILC2 Axis to Promote Allergic Airway Inflammation

Zhu

Cai

et al. 2022

Front. Immunol.

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Small proline-rich proteins (SPRRs), components of cornified cell envelope precursors, have recently been found to participate in airway diseases. However, their role in allergic airway inflammatory conditions remains unknown. Here, we explored the expression of SPRR3 in house dust mite (HDM)-sensitized/challenged mice and attempted to elucidate the regulatory role of SPRR3 in allergic airway inflammation. SPRR3 was identified via bioinformatics analysis of Gene Expression Omnibus (GEO) databases and further confirmed to be upregulated in the lungs of asthmatic mice. Knockdown of SPRR3 via the intratracheal route significantly inhibited eosinophils in bronchoalveolar lavage fluid (BALF) and suppressed the expressions of type 2 cytokines (IL-4, IL-5, and IL-13) in BALF and lung tissues. Further, SPRR3 knockdown reduced the expression of IL-33 and further attenuated the activation of the PI3K/AKT/NF-κB signaling pathway in the recruitment of group 2 innate lymphoid cells (ILC2s) to inhibit allergic airway inflammation. In vitro, SPRR3 siRNA could alleviate HDM-induced inflammatory responses in BEAS-2B cells. This study reveals the regulatory role of SPRR3 in allergic airway inflammation, identifying this protein as a potential novel therapeutic target for asthma.

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Increased epithelial galectin‐13 expression associates with eosinophilic airway inflammation in asthma

Cited by 10 publications

References 37 publications

PTPRH Alleviates Airway Obstruction and Th2 Inflammation in Asthma as a Protective Factor

PTPRH Alleviates Airway Obstruction and Th2 Inflammation in Asthma as a Protective Factor

CCCTC‐binding factor transcriptionally regulates Galectin‐7 and activates the JNK/STAT3 axis to aggravate bronchial epithelial cell injury

Small Proline-Rich Protein 3 Regulates IL-33/ILC2 Axis to Promote Allergic Airway Inflammation

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