Up‐regulation of FUT8 inhibits TGF-β1-induced activation of hepatic stellate cells during liver fibrogenesis

Kuang, Mengzhen; Wu, Hao; Hu, Lan; Guo, Xinying; He, Daochuan; Liu, Bo; Chen, Mengqian; Gu, Jie; Gu, Jianxin; Zeng, Xiaoqing; Ruan, Yuanyuan

doi:10.1007/s10719-021-09975-x

Cited by 7 publications

(3 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FUT8 is known to contribute to the exacerbation of AS, and oxLDL-induced upregulation of FUT8 is associated with decreased migratory activities of macrophages in AS [33]. Being the sole catalyzer of core fucosylation, FUT8 plays a crucial role in various diseases, including CVD and diabetes, where abnormal core fucosylation has been observed [34].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of LINC01128 Downregulates FUT8 to Inhibit OxLDL-Induced Vascular Smooth Muscle Cell Apoptosis in Atherosclerosis

Ni,

2024

Discovery Medicine

View full text Add to dashboard Cite

Background: The apoptosis of vascular smooth muscle cells (VSMCs) contributes to the progression of atherosclerosis (AS). Long intergenic non-protein codingRNA 1128 (LINC01128) has been implicated in AS, and this study aims to uncover the role and mechanism of LINC01128 in regulating oxidized low-density lipoprotein (oxLDL)-induced VSMCs. Methods: The position of LINC01128 in cells and its target genes were predicted using bioinformatics. The localization of LINC01128 in human VSMCs was determined through fluorescence in situ hybridization. VSMCs were transfected, and the interaction between LINC01128 and fucosyltransferase 8 (FUT8) was validated by chromatin immunoprecipitation assay. The apoptotic VSMC model was established using oxLDL. LINC01128 expression in VSMCs was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), and FUT8 expression was detected by qRT-PCR and western blot. VSMC viability, migration, invasion abilities, and apoptosis were assessed using cell counting kit-8, transwell assay, and flow cytometry, respectively. Results: OxLDL (200 µg/mL) upregulated the expression of LINC01128 and FUT8 mRNA, as well as FUT8 protein, in VSMCs. LINC01128 was expressed in the nucleus of VSMCs and bound to FUT8. Knockdown of LINC01128 alleviated the inhibitory effects of oxLDL (200 µg/mL) on viability, migration, and invasion, and mitigated the promotion of apoptosis and FUT8 expression in VSMCs. On the other hand, FUT8 overexpression enhanced the suppressive effects of oxLDL (200 µg/mL) on viability, migration, and invasion activities, and amplified the facilitating effect of oxLDL on apoptosis in VSMCs. Moreover, FUT8 overexpression reversed the impact of LINC01128 silencing on viability, migration, invasion, and apoptosis in oxLDL-stimulated VSMCs. Conclusion: The knockdown of LINC01128 downregulates FUT8, inhibiting the progression of VSMCs in AS.

show abstract

Section: Discussionmentioning

confidence: 99%

Knockdown of LINC01128 Downregulates FUT8 to Inhibit OxLDL-Induced Vascular Smooth Muscle Cell Apoptosis in Atherosclerosis

Ni,

2024

Discovery Medicine

View full text Add to dashboard Cite

show abstract

“…Reduced levels of FUT7 CpG DNA methylation have been found in lung cancer, especially in LUSC ( 118 ), and FUT7 promotes lung cancer proliferation by activation of the EGFR/AKT/mTOR signal pathway ( 119 ). FUT8, whose expression is upregulated in most cancers, regulates the core fucosylation of PD-1 ( 120 , 121 ), PD-L2 ( 122 ), TGF-β ( 123 ), TNFR ( 124 ), EGFR ( 78 , 125 , 126 ), B7H3 ( 127 ), α3β1 integrin ( 128 ), and E-cadherin ( 129 ) as well as that of mucins ( 130 ). Upregulated expression of FUT8 in cancer-associated fibroblasts promotes the construction of an invasive tumor microenvironment in NSCLC through the core fucosylation of EGFR ( 78 ).…”

Section: Glycoenzyme-based Protein Glycosylation Changes In Crdsmentioning

confidence: 99%

Targeting protein glycosylation to regulate inflammation in the respiratory tract: novel diagnostic and therapeutic candidates for chronic respiratory diseases

2023

View full text Add to dashboard Cite

Protein glycosylation is a widespread posttranslational modification that can impact the function of proteins. Dysregulated protein glycosylation has been linked to several diseases, including chronic respiratory diseases (CRDs). CRDs pose a significant public health threat globally, affecting the airways and other lung structures. Emerging researches suggest that glycosylation plays a significant role in regulating inflammation associated with CRDs. This review offers an overview of the abnormal glycoenzyme activity and corresponding glycosylation changes involved in various CRDs, including chronic obstructive pulmonary disease, asthma, cystic fibrosis, idiopathic pulmonary fibrosis, pulmonary arterial hypertension, non-cystic fibrosis bronchiectasis, and lung cancer. Additionally, this review summarizes recent advances in glycomics and glycoproteomics-based protein glycosylation analysis of CRDs. The potential of glycoenzymes and glycoproteins for clinical use in the diagnosis and treatment of CRDs is also discussed.

show abstract

“…Nonetheless, upregulation of FUT8 conversely inhibits TGF-β1-induced transdifferentiating as well as pro-fibrotic signal in HSCs. Upregulation of FUT8 quells HSCs stimulation in a negative feed-forward cycle as well as provides a possible curative maneuver to LF though focusing on FUT8 [52] .…”

Section: Other Roles With Smad Signaling Pathwaymentioning

confidence: 99%

Small-molecule natural products for reversing liver fibrosis based on modulation of HSCs activation: an update

Zheng

Yang

Luo

et al. 2022

Preprint

View full text Add to dashboard Cite

Liver fibrosis (LF) is a trauma repair process carried out by the liver in response to various acute and chronic liver injuries, featured by excessive proliferation as well as abnormal dismissal of extracellular matrix as the main pathological features, and its continuous development will deteriorate into cirrhosis, liver cancer as well as other illnesses. The occurrence of LF is closely related to Hepatic stellate cells (HSCs) stimulation, and intervention in HSCs proliferation is expected to reverse LF. Plant-based small molecule drugs have anti-LF effects, and their mechanisms of action are related to anti-inflammation, anti-oxidative stress, as well as inhibition of abnormal accumulation of extracellular matrix. Consequently, new agents for HSCs will be required to furnish a possible curative response. Small-molecule natural products might be attractive for LF therapy. That is because they not only have the effect against HSCs, but also have excellent qualities such as low toxic side effects and easy availability from the perspective of safety and cost. In this review, we provide an updated review of the signal transduction pathways involved in HSCs and small-molecule natural products targeting HSCs reported in the past 3 years at home and abroad, with the aim of providing new ideas for the development of plant-based small molecule drugs targeting HSCs to reverse LF.

show abstract

Up‐regulation of FUT8 inhibits TGF-β1-induced activation of hepatic stellate cells during liver fibrogenesis

Cited by 7 publications

References 53 publications

Knockdown of LINC01128 Downregulates FUT8 to Inhibit OxLDL-Induced Vascular Smooth Muscle Cell Apoptosis in Atherosclerosis

Knockdown of LINC01128 Downregulates FUT8 to Inhibit OxLDL-Induced Vascular Smooth Muscle Cell Apoptosis in Atherosclerosis

Targeting protein glycosylation to regulate inflammation in the respiratory tract: novel diagnostic and therapeutic candidates for chronic respiratory diseases

Small-molecule natural products for reversing liver fibrosis based on modulation of HSCs activation: an update

Contact Info

Product

Resources

About