Sialyltransferase activity of human plasma and aortic intima is enhanced in atherosclerosis

Gracheva, E. V.; Samovilova, N. N.; Golovanova, N. K.; Il’inskaya, O. P.; Tararak, E.; Malyshev, P.P.; Кухарчук, В. В.

doi:10.1016/s0925-4439(01)00093-x

Cited by 21 publications

(11 citation statements)

References 29 publications

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“…Previous studies have indicated that serum TSA concentrations are elevated in diabetes mellitus (both type 1 and type 2) with and without vascular complications (12). It is worth mentioning that a (37) reported elevated activity of sialyl transferase in aortic intimal and plasma in atherosclerosis. Since, sialyl transferase involves in different metabolic pathways for adding sialic acid to glycoproteins and glycolipids (12).…”

Section: Discussionmentioning

confidence: 92%

Triethylenetetramine reduces some blood parameters in alloxan-induced diabetes mellitus in New Zealand white rabbit: evidence for histopathologic effects

2016

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This study aimed to assess whether the triethylenetetramine (TETA) is impressed the plasma level of homocysteine (Hcy), total sialic acid (TSA) and cardiac troponin I (cTnI) as cardiovascular diseases risk factors, cystatin c (Cys c) and glucose along with histopathologic changes in alloxan induced diabetes mellitus in rabbit. Twenty number New Zealand white rabbits were assigned for this study. After induction of diabetes mellitus, TETA was orally administrated with different doses (10, 20, 40 mg/kg/day, A, B, C groups respectively) for 6 months daily and group D (as positive control) not received TETA. In the following, above parameters, insulin and glucose were measured in the all groups. Furthermore, histopathologic evaluation was carried out for aorta, kidney and pancreas in the all ones. Amounts of plasma cTnI, Hcy, TSA, Cys c and glucose concentrations decreased significantly (P < 0.01) in group C (40 mg/kg/day) compared with group D (positive control). In respect of insulin, normalizing of insulin occurred in group C (40 mg/kg/day) compared with group D (positive control). It is worth mentioning that during increasing of TETA dose, those levels decreased. In terms of histopathology, ameliorative and restoring effect of TETA on pancreatic beta-cells, glomeruli, renal tubules and aorta was determined in this study. The results suggested that TETA administration plays substantial role in tremendous alleviation of forenamed parameters and amelioration of beta-cells, renal glomeruli and tubules. Hence, TETA in the dose 40 mg/kg/day may utilize in the part of human diabetes mellitus management including cardiovascular, renal diseases and glucose normalizing.

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Section: Discussionmentioning

confidence: 92%

Triethylenetetramine reduces some blood parameters in alloxan-induced diabetes mellitus in New Zealand white rabbit: evidence for histopathologic effects

2016

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“…It has long been known that changes in the level of circulatory ST6Gal-1 and the circulatory sialyl-glycan structures constructed by ST6Gal-1 are associated with a diverse array of clinical conditions including stress (6), atherosclerosis(4, 34), alcoholism (35, 36), as well as in a certain cancers, particularly colon, breast cancers and multiple myeloma (10–12). Studies in the 1980's have established that elevated release of ST6Gal-1 into the blood was a component of the hepatic acute phase response (37, 38), although insight into the physiologic contribution of blood ST6Gal-1 remained largely elusive.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Sialyltransferase Infusion Mitigates Infection-Driven Acute Lung Inflammation

et al. 2019

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Inappropriate inflammation exacerbates a vast array of chronic and acute conditions with severe health risks. In certain situations, such as acute sepsis, traditional therapies may be inadequate in preventing severe organ damage or death. We have previously shown cell surface glycan modification by the circulating sialyltransferase ST6Gal-1 regulates de novo inflammatory cell production via a novel extrinsic glycosylation pathway. Here, we show that therapeutic administration of recombinant, bioactive ST6Gal-1 (rST6G) mitigates acute inflammation in a murine model mimicking acute exacerbations experienced by patients with chronic obstructive pulmonary disease (COPD). In addition to suppressing proximal neutrophil recruitment at onset of infection-mediated inflammation, rST6G also muted local cytokine production. Histologically, exposure with NTHI, a bacterium associated with COPD exacerbations, in rST6G-treated animals revealed consistent and pronounced reduction of pulmonary inflammation, characterized by smaller inflammatory cuffs around bronchovascular bundles, and fewer inflammatory cells within alveolar walls, alveolar spaces, and on pleural surfaces. Taken together, the data advance the idea that manipulating circulatory ST6Gal-1 levels has potential in managing inflammatory conditions by leveraging the combined approaches of controlling new inflammatory cell production and dampening the inflammation mediator cascade.

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“…Glycotransferases including sialyltransferases may also be expressed on cell surfaces2728. With respect to the vascular wall, sialyltransferase activity has been observed in membrane preparations containing the Golgi apparatus isolated from human aortic intima29. Expression of ST6GALNAC5 in murine (accession numbers in EMBI-EBI (http://www.ebi.ac.uk/expressionprofiler/): E-GEOD-775, E-GEOD-1479, and E-GEOD-24940) and human (E-GEOD-2240, E-GEOD-40231) heart cells, including human coronary artery cells (E-GEOD-3526), has been shown in several microarray experiments17.…”

Section: Discussionmentioning

confidence: 99%

Mutation in ST6GALNAC5 identified in family with coronary artery disease

InanlooRahatloo

Parsa

Huse

et al. 2014

Sci Rep

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We aimed to identify the genetic cause of coronary artery disease (CAD) in an Iranian pedigree. Genetic linkage analysis identified three loci with an LOD score of 2.2. Twelve sequence variations identified by exome sequencing were tested for segregation with disease. A p.Val99Met causing mutation in ST6GALNAC5 was considered the likely cause of CAD. ST6GALNAC5 encodes sialyltransferase 7e. The variation affects a highly conserved amino acid, was absent in 800 controls, and was predicted to damage protein function. ST6GALNAC5 is positioned within loci previously linked to CAD-associated parameters. While hypercholesterolemia was a prominent feature in the family, clinical and genetic data suggest that this condition is not caused by the mutation in ST6GALNAC5. Sequencing of ST6GALNAC5 in 160 Iranian patients revealed a candidate causative stop-loss mutation in two other patients. The p.Val99Met and stop-loss mutations both caused increased sialyltransferase activity. Sequence data from combined Iranian and US controls and CAD affected individuals provided evidence consistent with potential role of ST6GALNAC5 in CAD. We conclude that ST6GALNAC5 mutations can cause CAD. There is substantial literature suggesting a relation between sialyltransferase and sialic acid levels and coronary disease. Our findings provide strong evidence for the existence of this relation.

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Sialyltransferase activity of human plasma and aortic intima is enhanced in atherosclerosis

Cited by 21 publications

References 29 publications

Triethylenetetramine reduces some blood parameters in alloxan-induced diabetes mellitus in New Zealand white rabbit: evidence for histopathologic effects

Triethylenetetramine reduces some blood parameters in alloxan-induced diabetes mellitus in New Zealand white rabbit: evidence for histopathologic effects

Recombinant Sialyltransferase Infusion Mitigates Infection-Driven Acute Lung Inflammation

Mutation in ST6GALNAC5 identified in family with coronary artery disease

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