GLCCI1 reduces collagen deposition and airway hyper‐responsiveness in a mouse asthma model through binding with WD repeat domain 45B

Xun, Qiufen; Kuang, Jiu-long; Yang, Qing; Wang, Wei; Zhu, Guofeng

doi:10.1111/jcmm.16658

Cited by 7 publications

(3 citation statements)

References 29 publications

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“…reported that during the occurrence and development of asthma, GLCCI1 inhibited autophagy and promoted airway remodelling by inhibiting WDR45 expression, thus alleviating asthma [19] . Qiufen Xun et al reported that GLCCI1 inhibits airway remodelling and ameliorates asthma by inhibiting the IL-13/periostin/TGF-β1 pathway [16] .…”

Section: Discussionmentioning

confidence: 99%

The GLCCI1/STAT3 pathway: A novel pathway involved in diabetic cognitive dysfunction and the therapeutic effect of salidroside

Niu,

Xu,

Liu

et al. 2024

Preprint

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Diabetic cognitive dysfunction (DCD) is a complication of diabetes that seriously affects quality of life. Glucocorticoid-induced transcript 1 (GLCCI1) has been found to be involved in inflammation, apoptosis and autophagy in various diseases. However, the distribution of GLCCI1 in the brain and its role in DCD have not yet been revealed. In addition, the potential therapeutics effects of salidroside (SAL), a phenyl propyl glycoside compound known for its neuroprotective effects in treating DCD are unknow. In the present study, we found that GLCCI1 was localized in hippocampal neurons. C57BL/6J mice with DCD presented downregulation of GLCCI1 and Bcl-2 and upregulation of p-STAT3, Bax, Caspase-3 and Cleaved Caspase-3. Overexpression of GLCCI1 or SAL administration relieved DCD, reversed the changes in the expression of these cytokines, and alleviated morphological alterations in hippocampal neurons. Interestingly, SAL alleviated DCD and attenuated the expression of GLCCI1 and p-STAT3, showing similar effects as GLCCI1 overexpression. These findings suggest that the GLCCI1/STAT3 axis plays a crucial role in DCD and is involved in SAL-mediated attenuation of DCD.

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Section: Discussionmentioning

confidence: 99%

The GLCCI1/STAT3 pathway: A novel pathway involved in diabetic cognitive dysfunction and the therapeutic effect of salidroside

Niu,

Xu,

Liu

et al. 2024

Preprint

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“…It can reduce collagen deposition and airway hyper-responsiveness in a mouse asthma model through binding with WD repeat domain 45B and represses airway remodeling of the asthmatic mouse via inhibiting IL-13/periostin/ TGF-β1 signaling. In addition, the reduced methylation level of the GLCCI1 gene body in peripheral blood influences PI3k-Akt and MAPK pathways and it may be contributed to detect asthma and asthma severity, 16,28,29 which may further strengthen the understanding of the role and mechanism of GLCCI1 contributed to the pathogenesis of AR.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid-Induced Transcript 1(GLCCI1) SNP rs37937 Is Associated With the Risk of Developing Allergic Rhinitis and the Response to Intranasal Corticosteroids in a Chinese Han Population

Peng

Zhan

et al. 2023

Am J Rhinol�Allergy

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Background Evidence has shown that glucocorticoid-induced transcript 1 (GLCCI1) single nucleotide polymorphism (SNP) rs37937 is associated with asthma. Objectives The objective of this study was to investigate whether the GLCCI1 SNP rs37937 is a risk factor for allergic rhinitis (AR) in a Chinese Han population. Methods A total of 220 individuals including 109 AR patients and 111 healthy subjects were included. The genotyping of GLCCI1 rs37973 was performed by the SNaPshot method. The correlations of rs37973 polymorphism, AR risk, and clinical characteristics were further analyzed, as well as the treatment response to intranasal corticosteroids (INCS) in AR patients of different genotypes. Results Three GLCCI1 rs37973 SNP genotypes were identified in both AR patients and healthy subjects. Significant association between rs37973 polymorphism and AR under allele model, dominant model, heterozygote model, and homozygote model were shown. The A allele frequency of SNP rs37973 in AR was significantly higher than that in controls. The serum total immunoglobulin E (IgE) in AR patients of AA genotype was significantly higher than in patients of GA and GG genotype, and the serum total IgE in GA genotype was significantly higher than in GG genotype. Interestingly, after 4 weeks of INCS treatment for AR patients, the improvement of the nasal itching score, sneezing score, runny nose score, total nasal symptom score, and visual analog scale score of the GG genotype were worse than the AA or GA genotype. Conclusion The GLCCI1 rs37937 polymorphism is associated with the risk of developing AR and the response to INCS treatment in the Chinese Han population.

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“…Mechanistically, GLCCI1 promotes the binding between glucocorticoid receptor (GR) and GR-interacting protein 1 (GRIP1) but inhibits the recruitment of GRIP1 to interferon regulatory factors IRF1 and IRF3 ( Hu et al, 2021 ). In a mouse model of asthma GLCCI1 was shown to play a role in airway remodeling by modulating inflammatory signaling ( Xun et al, 2021a ; Xun et al, 2021b ). Interestingly, analysis of morbidity across the lifespan found a decreased risk of asthma in Down syndrome patients compared to general population or patients with other forms of intellectual disability ( Baksh et al, 2023 ).…”

Section: Understanding the Function And Regulation Of Dyrk1a Through ...mentioning

confidence: 99%

Insights from the protein interaction Universe of the multifunctional “Goldilocks” kinase DYRK1A

Ananthapadmanabhan,

Shows,

Dickinson

et al. 2023

Front. Cell Dev. Biol.

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Human Dual specificity tyrosine (Y)-Regulated Kinase 1A (DYRK1A) is encoded by a dosage-dependent gene located in the Down syndrome critical region of human chromosome 21. The known substrates of DYRK1A include proteins involved in transcription, cell cycle control, DNA repair and other processes. However, the function and regulation of this kinase is not fully understood, and the current knowledge does not fully explain the dosage-dependent function of this kinase. Several recent proteomic studies identified DYRK1A interacting proteins in several human cell lines. Interestingly, several of known protein substrates of DYRK1A were undetectable in these studies, likely due to a transient nature of the kinase-substrate interaction. It is possible that the stronger-binding DYRK1A interacting proteins, many of which are poorly characterized, are involved in regulatory functions by recruiting DYRK1A to the specific subcellular compartments or distinct signaling pathways. Better understanding of these DYRK1A-interacting proteins could help to decode the cellular processes regulated by this important protein kinase during embryonic development and in the adult organism. Here, we review the current knowledge of the biochemical and functional characterization of the DYRK1A protein-protein interaction network and discuss its involvement in human disease.

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GLCCI1 reduces collagen deposition and airway hyper‐responsiveness in a mouse asthma model through binding with WD repeat domain 45B

Cited by 7 publications

References 29 publications

The GLCCI1/STAT3 pathway: A novel pathway involved in diabetic cognitive dysfunction and the therapeutic effect of salidroside

The GLCCI1/STAT3 pathway: A novel pathway involved in diabetic cognitive dysfunction and the therapeutic effect of salidroside

Glucocorticoid-Induced Transcript 1(GLCCI1) SNP rs37937 Is Associated With the Risk of Developing Allergic Rhinitis and the Response to Intranasal Corticosteroids in a Chinese Han Population

Insights from the protein interaction Universe of the multifunctional “Goldilocks” kinase DYRK1A

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