Glycosyltransferases, glycosylation and atherosclerosis

Qin, Pu

doi:10.1007/s10719-014-9560-8

Cited by 29 publications

(13 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1, 2 The importance of glycosylation in immune regulation has also been clearly demonstrated, 2, 3, 7 and an increasing number of studies have highlighted the importance of protein glycosylation in the pathogenesis of atherosclerosis 24, 25 and cancer 4, 26 . The commonality of inflammation and immune function to the pathogenesis of diverse diseases including CVD and some cancers has also been demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Circulating N-Linked Glycoprotein Acetyls and Longitudinal Mortality Risk

Lawler

Akinkuolie

Chandler

et al. 2016

Circulation Research

104

View full text Add to dashboard Cite

Rationale Circulating glycoprotein N-acetyl glucosamine residues have recently been associated with incident cardiovascular disease (CVD) and diabetes mellitus. Objective Using a plasma glycan biosignature (GlycA) to identify circulating N-acetyl glycan groups, we examined the longitudinal association between GlycA and mortality among initially-healthy individuals. Methods and Results We quantified GlycA by 400 MHz 1H nuclear magnetic resonance (NMR) spectroscopy in 27,524 participants in the Women's Health Study (WHS; NCT00000479). The primary outcome was all-cause mortality. We replicated the findings in an independent cohort of 12,527 individuals in the JUPITER trial (NCT00239681). We also undertook secondary examination of CVD and cancer mortality in WHS. In WHS, during 524,515 person-years of follow-up (median 20.5 years) there were 3,523 deaths. Risk-factor adjusted multivariable Cox proportional hazard ratio (95% confidence interval) per standard deviation increment in GlycA for all-cause mortality was significantly increased at 5-years (1.21 [1.06, 1.40]) and during maximal follow-up (1.14 [1.09, 1.16]). Similar risk for all-cause mortality was observed in the replication cohort (1.33 [1.21, 1.45]). In WHS, risk of CVD mortality was increased at 5-years (1.43 [1.05, 1.95]) and during maximal follow-up (1.15 [1.04, 1.26]); and of cancer mortality at 5-years (1.23 [1.02, 1.47]) and during maximal follow-up (1.08 [1.01, 1.16]). Examination of correlations and mortality associations adjusted for hsCRP, fibrinogen, and ICAM-1, suggested that GlycA reflects summative risk related to multiple pathways of systemic inflammation. Conclusions Among initially-healthy individuals, elevated baseline circulating glycoprotein N-acetyl methyl groups were associated with longitudinal risk of all-cause, cardiovascular, and cancer mortality.

show abstract

Section: Discussionmentioning

confidence: 99%

Circulating N-Linked Glycoprotein Acetyls and Longitudinal Mortality Risk

Lawler

Akinkuolie

Chandler

et al. 2016

Circulation Research

104

View full text Add to dashboard Cite

show abstract

“…Although previous studies have focused on endothelial cell surface-bound chemokine expression in endothelial dysfunction and atherosclerosis development, cell adhesion molecules and chemokine receptors are also glycoproteins, thus suggesting that other regulatory mechanisms, such as post-translational glycosylation, may contribute to their activities33. Aberrant sialylation has been correlated with leukocyte arrest during inflammation3435.…”

Section: Discussionmentioning

confidence: 99%

TNF-α regulates the proteolytic degradation of ST6Gal-1 and endothelial cell-cell junctions through upregulating expression of BACE1

Deng

Zhang

Liu

et al. 2017

Sci Rep

Self Cite

View full text Add to dashboard Cite

Endothelial dysfunction and monocyte adhesion to vascular endothelial cells are two critical steps in atherosclerosis development, and emerging evidence suggests that protein sialylation is involved in these processes. However, the mechanism underlying this phenomenon remains incompletely elucidated. In this study, we demonstrated that treatment with the proinflammatory cytokine TNF-α disrupted vascular endothelial cell-cell tight junctions and promoted monocyte endothelial cell adhesion. Western blotting and Sambucus nigra lectin (SNA) blotting analyses revealed that TNF-α treatment decreased α-2, 6-sialic acid transferase 1 (ST6Gal-I) levels and downregulated VE-Cadherin α-2, 6 sialylation. Further analysis demonstrated that TNF-α treatment upregulated β-site amyloid precursor protein enzyme 1 (BACE1) expression, thus resulting in sequential ST6Gal-I proteolytic degradation. Furthermore, our results revealed that PKC signaling cascades were involved in TNF-α-induced BACE1 upregulation. Together, these results indicated that the proinflammatory cytokine TNF-α impairs endothelial tight junctions and promotes monocyte-endothelial cell adhesion by upregulating BACE1 expression through activating PKC signaling and sequentially cleaving ST6Gal-I. Thus, inhibition of BACE1 expression may be a new approach for treating atherosclerosis.

show abstract

“…Many (or perhaps most) chemokine receptors, including decoy receptors and viral receptor mimics, are heterogeneously N - and/or O -glycosylated, in some cases influencing receptor function [126,127,128,129,130,131,132,133,134,135]. For example, removal of sialic acid moieties from CCR5 significantly reduced the efficacy of signaling by chemokines at this receptor but had little effect on CCR5-mediated HIV-1 infection [134].…”

Section: Post-translational Modificationsmentioning

confidence: 99%

Mechanisms of Regulation of the Chemokine-Receptor Network

Stone

Hayward

Huang

et al. 2017

IJMS

232

240

View full text Add to dashboard Cite

The interactions of chemokines with their G protein-coupled receptors promote the migration of leukocytes during normal immune function and as a key aspect of the inflammatory response to tissue injury or infection. This review summarizes the major cellular and biochemical mechanisms by which the interactions of chemokines with chemokine receptors are regulated, including: selective and competitive binding interactions; genetic polymorphisms; mRNA splice variation; variation of expression, degradation and localization; down-regulation by atypical (decoy) receptors; interactions with cell-surface glycosaminoglycans; post-translational modifications; oligomerization; alternative signaling responses; and binding to natural or pharmacological inhibitors.

show abstract

Glycosyltransferases, glycosylation and atherosclerosis

Cited by 29 publications

References 63 publications

Circulating N-Linked Glycoprotein Acetyls and Longitudinal Mortality Risk

Circulating N-Linked Glycoprotein Acetyls and Longitudinal Mortality Risk

TNF-α regulates the proteolytic degradation of ST6Gal-1 and endothelial cell-cell junctions through upregulating expression of BACE1

Mechanisms of Regulation of the Chemokine-Receptor Network

Contact Info

Product

Resources

About