Role of Glycosylation in Vascular Calcification

Masbuchin, Ainun Nizar; Rohman, Mohammad Saifur; Liu, Ping Yen

doi:10.3390/ijms22189829

Cited by 14 publications

(15 citation statements)

References 141 publications

(200 reference statements)

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“…It is well accepted that glycosylation is the most abundant modification after translation of proteins and is associated with multiple cellular events, such as inflammation, carcinogenesis, and cancer metastasis [ 34 , 35 ]. Alteration of glycosylation is now regarded as a feature hallmark in several cancer progression [ 36 ]. Most proteins in the eukaryotic cells undergo the glycosylation process, so as the SND1.…”

Section: Discussionmentioning

confidence: 99%

N-Glycosylation on Asn50 of SND1 Is Required for Glioma U87 Cell Proliferation and Metastasis

Zhou

Zheng

et al. 2022

Journal of Immunology Research

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Staphylococcal nuclease domain-containing protein 1 (SND1) is an evolutionarily conserved multidomain protein, which has gained attention recently due to its positive regulation in several cancer progression and metastatic spread. However, the specific contribution of SND1 glycosylation in glioma remains uncertain. In the current study, we confirmed that SND1 was highly expressed in human glioma. Using site-directed mutagenesis, we created four predicted N-glycosylation site mutants for SND1 and provided the first evidence that SND1 undergoes N-glycosylation on its Asn50, Asn168, Asn283, and Asn416 residues in human glioma U87 cells. In addition, we found that removing the N-glycans on the Asn50 site destabilized SND1 and led to its endoplasmic reticulum-associated degradation. Furthermore, destabilized SND1 inhibits the glioma cell proliferation and metastasis. Collectively, our results reveal that N-glycosylation at Asn50 is essential for SND1 folding and trafficking, thus essential for the glioma process, providing new insights for SND1 as a potential disease biomarker for glioma.

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Section: Discussionmentioning

confidence: 99%

N-Glycosylation on Asn50 of SND1 Is Required for Glioma U87 Cell Proliferation and Metastasis

Zhou

Zheng

et al. 2022

Journal of Immunology Research

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“…Calcification inducers include phosphate, bone morphogenic protein (BMP)-2, 4, 6, transforming growth factor (TGF) β, alkaline phosphatase (ALP), and fibroblast growth factor 23 (FGF23). Calcification inhibitors comprise matrix Gla protein (MGP), fetuin-A, osteoprotegerin (OPG), and inorganic pyrophosphatase ( 6 ). The role of programmed cell death (apoptosis) in VC has been reviewed elsewhere ( 8 ).…”

Section: A Brief Overview and Update In The Mechanism Of Vascular Cal...mentioning

confidence: 99%

“…VC can be mediated by VSMC phenotype switching ( 6 ). Activation of PDGFR has been involved in VSMC phenotype switching through common transcription factors involved in osteoblast-like phenotype switching, such as Krüppel-like factor (KLF4) ( 37 ).…”

Section: Role Of Receptor Tyrosine Kinase In Cardiovascular Calcifica...mentioning

confidence: 99%

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The two facets of receptor tyrosine kinase in cardiovascular calcification—can tyrosine kinase inhibitors benefit cardiovascular system?

Masbuchin

Widodo

Rohman

et al. 2022

Front. Cardiovasc. Med.

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Tyrosine kinase inhibitors (TKIs) are widely used in cancer treatment due to their effectiveness in cancer cell killing. However, an off-target of this agent limits its success. Cardiotoxicity-associated TKIs have been widely reported. Tyrosine kinase is involved in many regulatory processes in a cell, and it is involved in cancer formation. Recent evidence suggests the role of tyrosine kinase in cardiovascular calcification, specifically, the calcification of heart vessels and valves. Herein, we summarized the accumulating evidence of the crucial role of receptor tyrosine kinase (RTK) in cardiovascular calcification and provided the potential clinical implication of TKIs-related ectopic calcification. We found that RTKs, depending on the ligand and tissue, can induce or suppress cardiovascular calcification. Therefore, RTKs may have varying effects on ectopic calcification. Additionally, in the context of cardiovascular calcification, TKIs do not always relate to an unfavored outcome—they might offer benefits in some cases.

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“…Vascular calcification is a process similar to bone formation, which is highly adjustable and active 1 , 2 . Its occurrence is related to the phenotypic transformation from human aortic smooth muscle cells (HASMCs) to osteoblasts caused by various stimulating factors such as hyperglycemia 3 , 4 , oxidative stress 5 and inflammatory response 6 .…”

Section: Introductionmentioning

confidence: 99%

3-Arylcoumarin inhibits vascular calcification by inhibiting the generation of AGEs and anti-oxidative stress

Pan

Wang

et al. 2022

Journal of Enzyme Inhibition and Medicinal Chemistry

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Objective This work aims to screen drugs for preventing and treating vascular calcification. Method: We screened a series of 3-arylcoumarins for the detection of vascular calcification-associated factors using human aortic vascular smooth muscle cells. Results We found that compounds 14 and 32 significantly inhibited alkaline phosphatase (ALP) activity similar to aminoguanidine hydrochloride (AGH) in a cellular model of AGEs-induced calcification. We also found that compounds 14 and 32 could significantly decrease the levels of factors such as AGEs, intracellular calcium ions, and total ROS in the calcified cell model. Further study indicates that compound 14 could significantly inhibit the expression of P-ERK1/2, PKC, NF-κB, RAGE and OPN proteins and increased the expression of SM22-α and PPAR-γ proteins in the calcified cells. Conclusion We speculate that compound 14 inhibits vascular calcification by inhibiting oxidative stress and inhibiting AGEs production, suggesting that 3-arylcoumarin derivatives are potential candidates for the treatment of vascular calcification.

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Role of Glycosylation in Vascular Calcification

Cited by 14 publications

References 141 publications

N-Glycosylation on Asn50 of SND1 Is Required for Glioma U87 Cell Proliferation and Metastasis

N-Glycosylation on Asn50 of SND1 Is Required for Glioma U87 Cell Proliferation and Metastasis

The two facets of receptor tyrosine kinase in cardiovascular calcification—can tyrosine kinase inhibitors benefit cardiovascular system?

3-Arylcoumarin inhibits vascular calcification by inhibiting the generation of AGEs and anti-oxidative stress

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