Neuraminidase 1 promotes renal fibrosis development in male mice

Chen, Qianqian; Liu, Kang; Shi, Ning; Ma, Gaoxiang; Wang, Peipei; Xie, Hua-Mei; Jin, Si-Jia; Wei, Tingting; Yu, Xiangyu; Wang, Yi; Zhang, Junyuan; Li, Ping; Qi, Lian‐Wen; Zhang, Lei

doi:10.1038/s41467-023-37450-8

Cited by 13 publications

(4 citation statements)

References 63 publications

(69 reference statements)

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“…E-cadherin is used in the diagnosis and prognosis of epithelial cancers as reduced expression is associated with tumors undergoing EMT [ 60 ]. Moreover, other studies have shown that the increased expression of Neu-1 promotes EMT through the reduction in E-cadherin markers [ 61 , 62 ]. To determine the influence of the CB1 agonists on the expression of E-cadherin, we examined the presence and levels of E-cadherin as a marker of EMT in SW-620 colorectal cancer cells.…”

Section: Resultsmentioning

confidence: 99%

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Functional Selectivity of Cannabinoid Type 1 G Protein-Coupled Receptor Agonists in Transactivating Glycosylated Receptors on Cancer Cells to Induce Epithelial–Mesenchymal Transition Metastatic Phenotype

Bunsick,

Matsukubo,

Aldbai

et al. 2024

Cells

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Understanding the role of biased G protein-coupled receptor (GPCR) agonism in receptor signaling may provide novel insights into the opposing effects mediated by cannabinoids, particularly in cancer and cancer metastasis. GPCRs can have more than one active state, a phenomenon called either ‘biased agonism’, ‘functional selectivity’, or ‘ligand-directed signaling’. However, there are increasing arrays of cannabinoid allosteric ligands with different degrees of modulation, called ‘biased modulation’, that can vary dramatically in a probe- and pathway-specific manner, not from simple differences in orthosteric ligand efficacy or stimulus-response coupling. Here, emerging evidence proposes the involvement of CB1 GPCRs in a novel biased GPCR signaling paradigm involving the crosstalk between neuraminidase-1 (Neu-1) and matrix metalloproteinase-9 (MMP-9) in the activation of glycosylated receptors through the modification of the receptor glycosylation state. The study findings highlighted the role of CB1 agonists AM-404, Aravnil, and Olvanil in significantly inducing Neu-1 sialidase activity in a dose-dependent fashion in RAW-Blue, PANC-1, and SW-620 cells. This approach was further substantiated by findings that the neuromedin B receptor inhibitor, BIM-23127, MMP-9 inhibitor, MMP9i, and Neu-1 inhibitor, oseltamivir phosphate, could specifically block CB1 agonist-induced Neu-1 sialidase activity. Additionally, we found that CB1 receptors exist in a multimeric receptor complex with Neu-1 in naïve, unstimulated RAW-Blue, PANC-1, and SW-620 cells. This complex implies a molecular link that regulates the interaction and signaling mechanism among these molecules present on the cell surface. Moreover, the study results demonstrate that CB1 agonists induce NFκB-dependent secretory alkaline phosphatase (SEAP) activity in influencing the expression of epithelial–mesenchymal markers, E-cadherin, and vimentin in SW-620 cells, albeit the impact on E-cadherin expression is less pronounced compared to vimentin. In essence, this innovative research begins to elucidate an entirely new molecular mechanism involving a GPCR signaling paradigm in which cannabinoids, as epigenetic stimuli, may traverse to influence gene expression and contribute to cancer and cancer metastasis.

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Section: Resultsmentioning

confidence: 99%

“…Cells 2024, 13, x FOR PEER REVIEW 13 of 24 through the reduction in E-cadherin markers [61,62]. To determine the influence of the CB1 agonists on the expression of E-cadherin, we examined the presence and levels of Ecadherin as a marker of EMT in SW-620 colorectal cancer cells.…”

Section: Synthetic Cb1 Cannabinoids Am-404 Aravnil and Olvanil Margin...mentioning

confidence: 99%

Functional Selectivity of Cannabinoid Type 1 G Protein-Coupled Receptor Agonists in Transactivating Glycosylated Receptors on Cancer Cells to Induce Epithelial–Mesenchymal Transition Metastatic Phenotype

Bunsick,

Matsukubo,

Aldbai

et al. 2024

Cells

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“…In their study, Su et al ( Su et al, 2017 ) highlighted kidney resident cells, specifically podocytes secrete IL-6 under certain conditions to promote proliferation; affecting the differentiation of kidney cells. The concentration of various inflammatory signalling pathways and diseases related to inflammation in CKD patients suggests a link between CKD pathogenesis and autoimmune irregularities, a viewpoint widely accepted among CKD researchers ( Berthier et al, 2012 ; Chen et al, 2023 ). Among them, viral infections, lipids, and atherosclerosis were positively correlated with CKD, which suggests that CKD patients are prone to cardiovascular and autoimmune diseases ( Gorenjak, 2009 ; Olechnowicz-Tietz et al, 2013 ), and the development of such diseases is closely related to immune responses.…”

Section: Discussionmentioning

confidence: 99%

Development and evaluation of a chronic kidney disease risk prediction model using random forest

Mendapara

2024

Front. Genet.

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This research aims to advance the detection of Chronic Kidney Disease (CKD) through a novel gene-based predictive model, leveraging recent breakthroughs in gene sequencing. We sourced and merged gene expression profiles of CKD-affected renal tissues from the Gene Expression Omnibus (GEO) database, classifying them into two sets for training and validation in a 7:3 ratio. The training set included 141 CKD and 33 non-CKD specimens, while the validation set had 60 and 14, respectively. The disease risk prediction model was constructed using the training dataset, while the validation dataset confirmed the model’s identification capabilities. The development of our predictive model began with evaluating differentially expressed genes (DEGs) between the two groups. We isolated six genes using Lasso and random forest (RF) methods—DUSP1, GADD45B, IFI44L, IFI30, ATF3, and LYZ—which are critical in differentiating CKD from non-CKD tissues. We refined our random forest (RF) model through 10-fold cross-validation, repeated five times, to optimize the mtry parameter. The performance of our model was robust, with an average AUC of 0.979 across the folds, translating to a 91.18% accuracy. Validation tests further confirmed its efficacy, with a 94.59% accuracy and an AUC of 0.990. External validation using dataset GSE180394 yielded an AUC of 0.913, 89.83% accuracy, and a sensitivity rate of 0.889, underscoring the model’s reliability. In summary, the study identified critical genetic biomarkers and successfully developed a novel disease risk prediction model for CKD. This model can serve as a valuable tool for CKD disease risk assessment and contribute significantly to CKD identification.

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“…Our study found that dipsacoside B ameliorated APAP-induced hepatotoxicity by prohibiting Neu1 [ 69 ]. The newest evidence supported that salvianolic acid B show strong ability to inhibit Neu1 activity during renal fibrosis development [ 70 ]. Interfering peptides (IntPep) targeting the transmembrane (TM) domains 2 of human membrane NEU1 has been proved to disrupt NEU1 dimerization and efficiently block the sialidase activity at the plasma membrane [ 71 ].…”

Section: Neu1 Inhibitormentioning

confidence: 99%

The role of sialidase Neu1 in respiratory diseases

Mei,

Li,

Wang

et al. 2024

Respir Res

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Neu1 is a sialidase enzyme that plays a crucial role in the regulation of glycosylation in a variety of cellular processes, including cellular signaling and inflammation. In recent years, numerous evidence has suggested that human NEU1 is also involved in the pathogenesis of various respiratory diseases, including lung infection, chronic obstructive pulmonary disease (COPD), asthma, and pulmonary fibrosis. This review paper aims to provide an overview of the current research on human NEU1 and respiratory diseases.

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Neuraminidase 1 promotes renal fibrosis development in male mice

Cited by 13 publications

References 63 publications

Functional Selectivity of Cannabinoid Type 1 G Protein-Coupled Receptor Agonists in Transactivating Glycosylated Receptors on Cancer Cells to Induce Epithelial–Mesenchymal Transition Metastatic Phenotype

Functional Selectivity of Cannabinoid Type 1 G Protein-Coupled Receptor Agonists in Transactivating Glycosylated Receptors on Cancer Cells to Induce Epithelial–Mesenchymal Transition Metastatic Phenotype

Development and evaluation of a chronic kidney disease risk prediction model using random forest

The role of sialidase Neu1 in respiratory diseases

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